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URING THE PAST 20 years, major advances in the intraoperative management of patients undergoing thoracoabdominal aortic aneurysm (TAAA) surgery have substantially reduced postoperative primary morbidity and mortality. At present, mortality rates after TAAA repair are estimated to be 5% to 10%, neurologic deficits 3% to 10%, renal failure 8% to 29%, and pulmonary complications 30% to 40%.1-4 Among the most feared complications of thoracic aortic aneurysm (TAA) and TAAA surgery are paraparesis and paraplegia, which are estimated to occur in 6% to 10% of patients who undergo TAA or TAAA repair. 5,6 Patients with these complications have a 20% greater risk of mortality than do patients without postoperative paraparesis or paraplegia. These patients, who are usually older, require intensive rehabilitation. A patient’s risk of postoperative paraparesis and paraplegia is determined by aneurysmal extent, acute dissection, cross-clamp time, preoperative renal dysfunction, previous aortic surgery, diabetes, and rupture.7 Improvements in TAAA repair procedures, including reduced cross-clamp time, distal aortic perfusion, and reattachment of intercostal arteries, have minimized critical ischemic times. Adjuncts such as cerebrospinal fluid (CSF) drainage, spinal cord monitoring, atrial femoral bypass, regional and systemic cooling, intrathecal papaverine, intraoperative use of naloxone, steroids and barbiturates, and the recognition and treatment of factors related to coagulopathy, have also been introduced. 8 The arterial circulation of the spinal cord consists of 2 interconnected sources: intrinsic and extrinsic. The intrinsic blood supply consists of a single anterior spinal artery (ASA), which courses along the ventral aspect of the cord and ultimately supplies the bulk of the cord substance through penetrating arteries, and paired posterior spinal arteries, which supply the remainder of the cord. This intrinsic circulation in turn receives its extrinsic blood supply via the radiculomedullary arteries, although the anatomic details of this supply vary among individuals. The principal extrinsic blood supply in the cervical and upper thoracic region comes from branches of the vertebral arteries; the thoracolumbar cord is supplied by intercostal and lumbar arteries, and the conus is supplied by the lateral sacral branches of the hypogastric vessels. There are 2 aspects of the spinal cord circulation that explain the risk of cord ischemia during TAAA repair. First, the diameter and continuity of the ASA vary along its length. Angiographic studies have shown that the ASA becomes extremely narrow cephalad to its anastomosis with the great radicular artery. Second, the human spinal cord is irregularly supplied by the radiculomedullary arteries because only few of them actually reach the cord substance. The thoracolumbar region is at the most risk for ischemic injury because this region is typically supplied by a single radiculomedullary artery, better known as the artery of Adamkiewicz or arteria radicularis magna. This artery has been shown to arise from T9 to T12 in about 75% of individuals. Because this area falls within the segment of the aorta that is clamped during reconstruction, clamping can compromise the blood supply to the cord. With proximal descending aortic cross-clamping, adequate spinal cord perfusion requires ASA patency, collateral circulation, and sufficient spinal cord perfusion pressure, defined as the difference between spinal artery pressure and CSF pressure. 9 During hypoxia and hypercarbia, autoregulation of spinal cord blood flow is lost and flow becomes linearly related to perfusion pressure. For this reason, adjuncts that decrease CSF pressure will increase spinal cord perfusion pressure. The rationale for using a CSF drain is based on experimental data showing that (1) CSF pressure increases during aortic clamping and (2) reducing CSF pressure improves spinal perfusion. Drenger et al 10 observed acute increases in CSF pressure immediately after applying the aortic clamp during TAAA repair. These increases were similar in patients with and without distal bypass and have been attributed to a sudden elevation of cerebral blood flow. The authors also observed a second peak

Direct emergence of a dorsospinal artery from the aorta is a rare anatomic variant, of which a total of seven cases have been reported. This report offers an additional angiographic observation and reviews the literature.Two observations of common intercostal trunks documented during spinal angiography are described.In the first observation, the common intercostal trunk provided complete blood supply to two adjacent vertebral levels (T11 and T12). In other words, the trunk included an intercostal branch and a dorsospinal branch for each level. In the second observation, the common intercostal trunk provided an intercostal branch for each level (T9 and T10), but only one dorsospinal branch (T10). An isolated dorsospinal artery (DA) originated separately from the aorta at the T9 level, and provided a significant contribution to the anterior spinal axis.The two reported cases illustrate the concept of "complete" versus "incomplete" common intercostal trunks. In instances where an incomplete trunk is documented, a separate DA originating directly from the aorta must be looked for. A review of the literature indicates a tendency for isolated DAs to participate in the blood supply to the spinal cord.

Although identification of the key artery that perfuses the spinal cord is essential to avoid occurrence of paraplegia after surgery on the thoracoabdominal aorta, reliable and noncomplicated measures are not yet available. A new method of determining it by using echocardiography with a saline injection into the lumbar artery was evaluated for feasibility and adequacy in a canine model. In two mongrel dogs, the abdominal aorta was opened and saline was directly injected into the lumbar arteries while the spinal cord was visualized by echocardiography through the intervertebral disc. When the echogenic or Doppler signal was detected in the spinal cord, the particular lumbar artery was determined as "positive", or as "negative" when the signal was not detected. After the dog was sacrificed, red resin was injected into the "positive" arteries and blue resin into the "negative" arteries. In the extracted spinal cord, the anterior and posterior spinal arteries were filled with red resin, rather than with blue resin, to indicate that the key arteries were correctly identified. There were multiple "positive" arteries, which were mainly located on the left side and accounted for approximately one-third of the entire lumbar arteries. The "negative" arteries mainly perfused the muscles around the vertebra. Injected resin came out of the adjacent lumbar arteries of the same category, suggesting that communication is present among the positive arteries, but independently of that among the negative arteries. Echo-guided identification of key arteries is technically feasible and correctly determines the key arteries in this preliminary canine model.

CT and MRI have the potential to become useful adjuncts to forensic autopsy in the near future. The examination of fatal injuries facilitates a profound experience in the clinical-radiological examination of these cases; the more severe findings in corpses with autopsy verification can help one to understand the tiny signs seen in clinical cases of surviving victims. We present the case of a 44-year-old male diver who died from severe decompression sickness after rapid ascent from approximately 120 m. Post-mortem CT and MRI studies of the brain and spinal cord revealed extensive gas inclusions in cerebral arteries, spinal arteries and cerebrospinal fluid (CSF) spaces, while the intracranial venous sinuses remained unaffected. These findings were confirmed at autopsy. Appropriate imaging techniques can help forensic pathologists to aim their autopsies at findings that might otherwise remain undetected.

Dear Editor, Vertebral artery variations at the level of C1-2 have been documented, especially in patients with Down’s syndrome [5]. Additionally, cranio-vertebral junction (CVJ) anomalies are often seen in patients with Down’s syndrome [2]. The origin of posterior inferior cerebellar artery (PICA) at the level of C1-2 is one of the variations, with a reported incidence of approximately 1.1 % in normal population [4]. Of interest, such a variation of PICA has not been reported in CVJ anomaly with Down’s syndrome. It is important to identify such variation preoperatively to avoid complication during surgery for CVJ. A 7-year-old girl with Down’s syndrome presented with spastic quadriparesis that progressed over 6 months. X ray CVJ showed os-odontoideum with atlanto-axial dislocation reducing on extension (Fig. 1). Computed tomography (CT) Angiogram (2D and 3D reconstructed) images revealed the right PICA originating at the C1-2 level and crossing the joint space (Fig. 1). The patient underwent a posterior fusion. Intraoperatively, the bilateral C2 ganglion was cut. The vertebral artery (VA) could be seen coursing above the C1 arch, whereas the PICA was seen originating from VA between C1 and C2 transverse foramina and then crossing the C1-2 joint on the right side to course beneath the C1 arch. The vessel was carefully dissected, taking care not to injure it. The facetal surfaces were drilled lateral after retracting the PICA gently away from it. The lateral mass screws were inserted in C1, retracting the vessel gently to avoid injury. C2 pars-interarticularis screws were inserted and fused to C1 lateral mass screws. Bone grafts placed between the C1-2 joint and decorticated surface helped achieve a strong bony fusion. Her myelopathy improved significantly after 3 months. The PICA may originate extra-durally and extra-cranially in about 5–20 % [1]. An extradural PICA may arise just outside the dura at the CVJ or laterally above the transverse foramen of the atlas or between the transverse foramina of C-2 and C-1 [1]. In the normal population, the incidence of PICA originating between C2 and C1 transverse foramina is 1.1 % [4]. However, the incidence of other origins of PICA could not be localized in literature. Additionally, both CVJ and Vertebral artery (VA) abnormalities are more often seen in patients with Down’s syndrome as compared to those without it [2, 5]. Of interest, a anomalous PICA with CVJ abnormality in Down’s syndrome has never been described in the past. The variations in VA and origin of PICA is thought to be the result of variations in the development of the lateral spinal artery (LSA) and posterior spinal artery (PSA). The anterior or posterior location of the PICA (C2 origin) at the foramen magnum origin and the absence or presence of separate LSA help to distinguish the LSA from the PSA variant [3]. It has been suggested that chromosomal abnormality in Down syndrome contributes to VA abnormalities at CVJ [5]. After originating from the VA beyond the C2 transverse foramina, the PICA crosses across the posterior aspect of C1-2 joint to enter the dura at the level of C1. Such an origin and course of PICA makes it susceptible to injury during surgery, for the CVJ especially, while the C1-2 facet is being dissected, distracted and fixed with lateral mass screws. The abnormal PICA may be injured directly or its handling may tear its origin from the VA. Occasionally, the VA may end as this abnormal PICA [4]. The neurological damage due to PICA injury depends on the area it supplies. Although extradural PICAs do not send perforating branches to the anterior surface of the medulla P. Salunke (*) : S. Futane Department of Neurosurgery, PGIMER, Sector 12, Chandigarh, India 1600l2 e-mail: drpravin_salunke@yahoo.co.uk

Background. The purpose of this study was to determine whether the artery of Adamkiewicz (ARM) can be detected by magnetic resonance angiography and to determine the usefulness of preoperative magnetic resonance angiography evaluation of the ARM. Methods. Between April 2000 and December 2003, 120 patients underwent magnetic resonance angiography for detection of the ARM. The morphology of the anterior spinal artery at the ARM junction, as revealed by magnetic resonance angiography, in 99 patients in whom ARM was preoperatively detected was classified into the following three types: noncontinuation of the anterior spinal artery above the ARM junction (type A), continuation of the anterior spinal artery above and below the ARM junction (type B), and noncontinuation of the anterior spinal artery below the ARM junction (type C). Results. The ARMs were detected in 99 (83%) of 120 patients, and from a total of 110 ARMs 105 (95%) originated from intercostal arteries branching from the left side and 94 (86%) originated between Th9 and Th11. Two ARMs were found in 11 (11%) of 99 patients in whom ARMs were detected. In 107 patients, who underwent magnetic resonance angiography to reveal the morphology of the anterior spinal artery at the ARM junction, the patterns of the anterior spinal artery were type A in 59 patients (55%), type B in 21 patients (20%), type C in 3 patients (3%) and not classified in 24 patients (22%). No spinal cord injury occurred in patients in whom the ARM had been preoperatively detected. Conclusions. Preoperative detection of the ARM is possible by magnetic resonance angiography and is very useful for reducing the incidence of ischemic injury of the spinal cord.

Introduction/Purpose Retrospective study of spinal angiography and management of spinal arterio-venous malformations, at the department of Neuroradiology, Neurosciences Center, All India Institute of Medical Sciences, New Delhi, India, between 1989 and June 2011. Materials and Methods 190 patients were analyzed. 17 were negative angiograms. Four had spinal tumors. Arterio-venous spinal malformation was diagnosed in 169 patients. Results Among these 169 patients, 51 (30.2%) had spinal dural arteriovenous fistulae (SDAVFs), 48 (28.4%) had spinal cord arteriovenous malformations (SCAVMs), 58 (34.3%) had spinal cord arteriovenous fistulae (SCAVFs), 9 (5.3%) had epidural arteriovenous fistulae and 3 (1.8%) miscellaneous lesions. Overall preponderance of males (75%) was observed. SCAVF was the most common vascular lesion in our series. 90% of SDAVF patients were male. Most had progressive symptoms of motor weakness (96%), sensory deficits (90%) and sphincter disturbances (88%). Dorso-lumbar (D6–L2) location common, except one fistula at foramen magnum. In four patients, there were two fistulae each, two of them metachronous and two of them synchronous. Mean time to diagnosis in SDAVF was 12.9 months. 34 SDAVF patients were treated by surgery which improved or stabilized the clinical status in 88.5% & 3 (11.5%) deteriorated after surgery. Embolization was successful in 58% patients attempted & all improved with no recurrence. SCAVFs (58) outnumbered SCAVMs (48). Macro SCAVFs were preferentially treated by embolization and all except one improved. 60% Micro-AVFs treated by embolization and 93% of them improved. On the other hand 33% Micro-AVFs worsened after surgery. Three out of seven radicular fistulae treated by embolization improved clinically. Surgery was preferred for filar fistulae and 90% improved. Mean age of presentation for SCAVM was 25 years and 31.25% of them were younger than 20 years. 33% had acute however MR evidence of haematomyelia was seen in only 10%. 75% were Glomus type, 16.5% Multimyelomeric and four (8.5%) had Metameric malformations. 56% focal cord lesions occurred in dorso-lumbar region. Conus AVMs were between 21 and 30 years. Three out of four metameric lesions involved cervical segments. Venous ectasia, pial venous reflux and arteriovenous micro-fistulae were dominant angiographic features in SCAVMs. Aneurysm or pseudo-aneurysms were observed in 31.25% of cases. Out of 35 SCAVMs, 29 (83%) were treated by embolization with improvement or stabilization in 86%. 90% or more nidus obliteration could be achieved in 13 (44.83%), 80-90% in 7 (24.14%), 60-80% in 5 (17.24%) and 40%–60% in 4 (13.79%). Surgery improved or stabilized five out of six SCAVMs and one deteriorated. Six epidural AVMs and three vertebra-venous (VVF) fistulae were treated by embolization with cure of VVFs. Epidural AVMs typically required multiple sessions. Two spinal artery aneurysms in collateralized spinal artery were treated by coiling. Conclusion Endovascular treatment is effective in treating majority of spinal vascular lesions. Surgery can be reserved for selective situations like filar AVFs, lesions with unfavorable for endovascular embolizations and failed embolizations. Competing interests None.

A 39-year-old man presented with acute headache and neck pain, followed by quadriparesis and quadriparesthesia, accompanied by urinary and bowel incontinence. Lumbar puncture showed subarachnoid haemorrhage. Angiogram via a right axillary approach revealed severe coarctation of the aorta, between the left common carotid artery and left subclavian artery. Multiple collateral circulation including an enlarged anterior spinal arterial axis bridging the stenosed arch provided collateral circulation to the abdominal aorta. A small lobulated aneurysm was seen at the radiculomedullary-anterior spinal artery junction from the right ascending cervical artery. This patient underwent successful surgical clipping of the aneurysm. Pathogenesis of the spinal arterial aneurysm associated with coarctation of the aorta is likely to result from the haemodynamic stress from collateral circulation through the anterior spinal axis rather than segmental arterial disease or angiodysplastic disease. Aneurysms of the spinal artery are rare but can be unusually found in association with SCAVMs, coarctation of aorta, Klippel-Trenaunay syndrome or more rarely with aortic arch interruption.

Dear Editor,Due to the nonspecific nature of clinical symptoms, there isa long delay between onset of first symptoms and definitivediagnosis of SDAVF often. We report the case of a patientwith congestive myelopathy believed to be caused by alarge pelvic arteriovenous malformation, which concealed athoracic SDAVF.Case reportA 62-year-old man presented with progressive myelopathy.T2-weighted MRI of the entire spinal cord revealed a highintramedullary signal from Th7-Th9, accompanied byintradural dilated perimedullary vessels. These finding areconsistent with dural arteriovenous fistulas; therefore,selective spinal angiograms (DSA) were performed. How-ever, two DSAs failed to reveal any SDAVF; but, a largepelvic arteriovenous malformation (pAVM), with feedersfrom the internal iliac arteries and massively dilateddraining veins into the inferior caval vein, was incidentallyfound. Following the assumption that the pAVM waspossibly obstructing the drainage of the spinal veins therebycausing congestive damage to the spinal cord, it wasdecided to perform a partial embolization of the AVMbecause a complete embolization or surgical removal wasbelieved to harm the patient. However, several partialembolizations failed to relieve his symptoms. Thereafter,the patient was referred to our department for re-evaluation.A further spinal DSA failed to detect any SDAVFs.Therefore, we performed a complete embolization of thepAVM followed by surgical shunt disconnection. Hissymptoms regressed.Two months later, his symptoms progressed again. MRIshowed congestive changes of the cord. A pelvic angio-gram showed no revascularization of the pAVM. By then,due to the matching clinical signs and MRI findings, anSDAVF became highly suspicious again. However, aSDAVF was not detected by two complete spinal DSAs.Finally, using a multidetector computed tomographicangiography (MDCTA), at Th3 an arteriovenous fistulawas revealed. The feeder was from the sixth spinal artery,which sprouted from a bronchial artery that originated fromthe thoracic aorta a few millimeters above the seventhspinalartery(Fig.1). Therefore, this bronchial artery was notdetected by spinal angiography because the neuroradiologist,not expecting such an anatomic anomaly, was able tocatheterize the seventh spinal artery, only. The MDCTAfinding was then confirmed by a targeted DSA (Fig. 1).Finally, the fistula was clipped and the patient’ssymptomswere regressive.Six months later, the patient presented again with aprogressive myelopathy. MRI revealed an enlargement ofthe T2-signal intensity of the thoracic spine but without anyperimedullary dilated veins. A MDCTA did not show anysigns of a SDAVF recurrence. CSF and blood laboratoryexams found no evidence for any inflammation or

A 40-year-old man with known definite Behçet's disease (BD) was admitted with confusional state which had started 4 days before admission with an acute headache and vomiting. Neurological examination revealed confusion, stiff neck, right facial weakness, left hemiparesis, dysartria and truncal ataxia. CSF was haemorrhagic and xanthochromic. Cranial CT scans were negative, but MRI showed a right pontine hyperintense lesion on T2-weighted images. Bilateral carotid angiograms were normal. Right vertebral angiogram showed findings consistent with a dissection at the V2 segment of the artery. At the level of the fifth cervical vertebra, a radiculomedullary branch of the vertebral artery with an aneurysmal dilatation in its intradural portion was notable. This case shows that, in BD, aneurysm formation can also occur in a spinal artery and spontaneous vertebral artery dissection can be seen.

Major hemoptysis is a potentially life-threatening complication of cystic fibrosis (CF) lung disease. Bronchial artery embolization (BAE) along with treatment of a CF pulmonary exacerbation has become the most widely used therapeutic approach for major hemoptysis in CF. However, BAE has been associated with severe complications, especially when bronchial artery to spinal artery anastomoses are present. This case study describes the successful treatment of major hemoptysis in CF with tranexamic acid, in an individual in whom 12 previous BAE procedures had been performed and further procedures were contraindicated secondary to bronchial artery to spinal artery collaterals. Recurrence of the hemoptysis occurred after attempts had been made to withdraw the tranexamic acid. Tranexamic acid was resumed with resolution of the hemoptysis, and the therapy has been used continuously for 13 months without any complications.

Previous reports suggest a generally successful experience with embolotherapy of vertebral arteriovenous fistulas of the neck. However, potential complications do exist, as shown by this report documenting spinal cord ischemia secondary to compromise of a dominant spinal artery arising from the proximal aspect of the right vertebral artery.

✓ The case is presented of an isolated intramedullary posterior spinal artery aneurysm at the C-2 level in a 3-year-old girl. Quadriplegia related to probable intramedullary hemorrhage was the presenting symptom. Magnetic resonance imaging revealed findings consistent with an intramedullary vascular lesion, and vertebral angiography confirmed this to be an aneurysm of the posterior spinal artery. No associated vascular abnormalities were noted, and the aneurysm was successfully resected. Previous reports of isolated spinal aneurysms are reviewed.

Background . Reattachment of segmental arteries is one method used to prevent paraplegia associated with thoracoabdominal aortic repair. Nevertheless, even when important segmental arteries are reattached, ischemia causing spinal injury may occur during anastomosis. Methods . In 27 patients undergoing thoracoabdominal aortic repair, we attempted to perfuse the segmental arteries to be reattached with catheters connected to the distal bypass circuit. To identify perioperative risk factors for spinal ischemia, we examined changes in spinal somatosensory evoked potentials. Results . A median value of four segmental arteries were perfused in 20 (74%) of the 27 patients. Changes in somatosensory evoked potential indicative of spinal ischemia were observed in 13 patients (48%). The only risk factor associated with changes in evoked potentials revealed by a multivariate analysis was prolonged aortic cross-clamp time (> 120 minutes). Of the 2 patients who suffered paraplegia, one had the longest clamp time and the other showed spinal cord necrosis due to embolic shower. Conclusions . Despite selective perfusion of segmental arteries, spinal ischemia associated with aortic cross-clamping may occur when clamping is prolonged over 120 minutes. Most of the changes appear to be reversible, however.

Objective Presentation of a patient with acute subarachnoid hemorrhage from a ruptured spinal artery aneurysm attributable to exacerbated Sjogren syndrome. Clinical presentation A 46-year-old woman with symptoms of exacerbated Sjogren syndrome experienced the acute onset of extreme headache accompanied by nuchal rigidity. Intervention A computed tomographic scan revealed subarachnoid hemorrhage. Angiography showed an isolated aneurysm of a branch of the right vertebral artery that was a feeding artery of the anterior spinal artery. Neither operative clipping nor endovascular coiling of the aneurysm was reasonable, owing to the high risk of occluding the anterior spinal artery during the intervention. Further diagnostic measures confirmed Sjogren syndrome and revealed cryoglobulinemic vasculitis, membranoproliferative glomerulonephritis with acute renal failure, Hashimoto thyroiditis, and acute hydrocephalus. In the course of conservative treatment, the patient recovered completely from the subarachnoid hemorrhage. One year after treatment with glucocorticoids and immunosuppressive agents, both the aneurysm and the vasculitis could no longer be detected on conventional angiography. Conclusion Generally, spinal artery aneurysms are exceptionally rare, and few cases of rupture with subsequent subarachnoid hemorrhage have been published. We report on a ruptured spinal aneurysm attributable to Sjogren syndrome-associated cryoglobulinemic vasculitis. Conservative treatment with glucocorticoids and immunosuppressive agents led to resolution of the vasculitic spinal aneurysm.

Spontaneous haematomyelia (intramedullary spinal haematoma), is an uncommon event. Predisposing conditions have been reported including syringomyelia, pregnancy and delivery, angioma, spinal artery aneurysm, and haemophilia, but only rarely has a pathological evaluation been performed. Two such cases studied at necropsy are reported. In one case, the haematoma was restricted to the cervical spinal cord, while in the second case it extended from the medulla into the lowest thoracic cord segments. In both cases the haematomyelia was fatal. In the first case the clinical course was subacute, but in the other the course was more acute. Careful neuropathological examination showed no apparent cause for the haemorrhages.

A 62-year-old woman developed headache, vomiting and fever. On admission to hospital, she showed an imparied level of consciousness, diplopia on left lateral gaze, bilateral hearing loss and left hemiparesis. Cranial contrast computed tomography (CT) revealed basal meningeal enhancement. Lumbar cerebrospinal fluid (CSF) showed an increase in cell count (80/mm3) and total protein (3000 mg/dl), and a decrease in glucose (65 mg/dl) in comparison with blood sugar (173 mg/dl). Polymerase chain reaction was positive for Mycobacterium tuberculosis in the CSF. She was diagnosed as having tuberculous meningitis and was treated with anti-tuberculous chemotherapy. Her level of consciousness recovered and other clinical signs improved gradually the first month after admission. However, in spite of the combination of anti-tuberculous chemotherapy and steroid therapy, her combination of anti-tuberculous chemotherapy and steroid therapy, her consciousness level worsened again in association with paraplegia at the sixth week after admission and magnetic resonance imaging (MRI) revealed multiple tuberculomas, spinal arachnoiditis and spinal cord infarction. On T2-weighted imaging some of the tuberculomas showed a central hyperintense area (a central bright core) with an isointense periphery, which was surrounded by a hyperintense area. The lesion appeared hypointense with an isointense rim on T1-weighted imaging, showing a ring enhancement on post-contrast T1W imaging. The spinal cord infarction was situated at the third thoracic cord, which corresponded to the borderline of spinal artery perfusion. This is a rare case of progression of spinal arachnoiditis and spinal cord infarction during anti-tuberculous chemotherapy, and who had tuberculoma with a central bright core on MRI.

Isolated rabbit spinal resistance-sized arteries (approximately 100 microns in diameter and approximately 3 mm long) were cannulated at both ends with glass micropipettes and perfused at constant pressure (60 mmHg). An increase of flow rate corresponding to a change of pressure gradient (delta P) ranging from 0 to 20 mmHg produced a flow-dependent vasodilation. Treatment with 50 microM aspirin or 10 microM indomethacin produced a significant reduction of the flow-dependent vasodilation only at delta P of 5 mmHg. In contrast, treatment with N omega-nitro-L-arginine methyl ester (L-NAME, 30 microM) produced no significant change. In the presence of 10 microM indomethacin, however, 30 microM L-NAME caused a marked decrease in the arterial diameter at delta P of 5 mmHg, which was completely reversed with additional administration of 1 mM L-arginine. Acetylcholine (ACh) produced a dose-dependent increase in the arterial diameter. The ACh-induced vasodilation was significantly reduced by 10 microM indomethacin or 50 microM aspirin and partially suppressed by 30 microM L-NAME. Pretreatment with both indomethacin and L-NAME completely reduced the ACh-induced vasodilation. In the presence of 10 microM indomethacin, additional treatment with 1 mM L-arginine significantly reversed the L-NAME-induced inhibition of the ACh-mediated vasodilation. Endothelial removal with Triton X-100 significantly reduced the ACh-induced vasodilation. Isocarbacyclin (a stable prostaglandin I2 analogue), prostaglandin E2, and arachidonic acid caused a dose-dependent dilation in the small arteries. These findings suggest that prostanoids play a major role in the flow- or ACh-induced vasodilation in the rabbit spinal resistance-sized small arteries.

Study Design. The results of preoperative selective spinal angiography were compared with intraoperative occlusion of segmental arteries and somatosensory-evoked potential monitoring during anterior spinal surgery. Objectives. To determine if temporary occlusion of major radicular vessels supplying the spinal cord would result in intraoperative somatosensory-evoked potential changes. Summary of Background Data. Temporary occlusion of segmental spinal arteries with concomitant somato-sensory-evoked potential monitoring has been used during anterior spinal surgery to avoid intraoperative vascular paraplegias caused by permanent ligations of vessels critical to the blood supply of the spinal cord. Methods. Preoperative selective spinal angiography was performed in 16 patients to identify important radicular arteries supplying the spinal cord. At the time of anterior spinal surgery, temporary occlusion of segmental vessels was accomplished with somatosensory-evoked potential monitoring. Results. Thirty-two radicular arteries were identified by arteriography in 16 patients. Temporary occlusion of nine segmental arteries in the surgical field supplying these radicular vessels resulted in no somatosensory-evoked potential changes. Results. Thirty-two arteries were identified by arteriography in 16 patients. Temporary occlusion of nine segmental arteries in the surgical field sypplying these radicular vessels resulted in no somatosensory-evoked potential changes. Conclusions. The lack of somatosensory-evoked potential changes after temporary occlusion of segmental arteries form which radicular arteries supply the spinal cord demonstrates sufficient perimedullary collateral circulation in that area of the spinal cord.

Abstract 1155 Introduction. Anterior spinal artery thrombosis (AST) results in sudden, often irreversible sensory and motor loss, with partial or complete paraplegia. This is recognized as a complication of: prothrombotic states; right to left shunting; trauma and spinal surgery. Both venous and arterial thrombosis, including the central nervous system, are well-recognized risks in sickle cell disease (SCD) but AST has not been described. In thalassemia disorders (Thal), cerebral infarction, often silent, is increasingly recognized (Mussalam et al, Thromb Res, Aug 2012). However AST is not a recognized complication. Here we describe four cases of acute onset AST in adults (3 Thal major, 1 SCD), leading to severe neurological irreversible or partially reversible deficits. Patients and Methods. Patients described were attending outpatients for monitoring drawn from two large adults clinics in the UK (UCLH, Whittington, over 1500 hemoglobinopathy patients) and Italy (Ospedale Maggiore Policlinico, Milan, 400 patients). All events occurred within a 3 year period. Results. Presenting symptoms and Magnetic Resonance Imaging (MRI) findings are shown in the Table. All cases presented acutely with a sensory level on examination and with bladder dysfunction. Three presented with motor weakness of both lower limbs (1 case initially in one limb). Case 3 presented with a sensory deficit affecting the sacral region but no motor deficit. Partial reversibility occurred in cases 1 and 3. In Thal cases, no prodromal syndrome and no prior history of thrombosis were seen. MRI showed changes consistent with acute cord ischemia (delayed in case 4 until 5 days). Extra-medullary hematopoiesis was demonstrated by MRI only in case 2, but was not sufficient to cause cord compression. Cerebrospinal fluid analysis was normal in all cases. Concomitant risk factors such as autoimmune markers, active hepatitis, trauma, or demonstrable prothrombotic markers other than those expected in SCD or Thal were not detected. In none of the Thal cases was a thrombotic history elicited but the SCD patient had a history of retinal artery and renal artery thrombosis (1 year previously). Discussion. A case series of this serious complication has not been previously reported. The known prothrombotic tendency in SCD and Thal is the most likely risk factor as other risk factors were absent. Thal cases were transfusion dependent, where thrombosis risk is generally about a quarter of that in non transfusion dependent Thal (Cappellini, Blood Reviews, 265, 2012, S20–23). In the SCD case, the prior history of arterial thrombosis, consistent with an embolic etiology, led us to examine whether a patent foramen ovale (PFO) was present, which was confirmed by bubble jet studies. This was subsequently closed. In patients with a history of embolic thrombosis, the presence of PFO should be sought and closure considered. Two cases were treated with Methylprednisolone soon after presentation. Two cases were commenced on Aspirin 75mg once a day to limit extension and as secondary prevention. The use of thrombolytic agents such as tissue thromboplastin activator have not been described in AST. In conclusion, spinal cord ischemia should be considered when facing a Thal or SCD patient with acute neurological symptoms affecting legs or bladder. This may be more common in hemoglobin disorders than is apparent from the literature. Table . Case 1 Case 2 Case 3 Case 4 Age at presentation 24 37 32 27 Gender Male Male Female Female Diagnosis SCD Thal Major Thal Major Thal Major Presentation symptoms Bilateral leg weakness Paraparesis Paraplegia Urine retention Sacral paraesthesia Urine retention Lower limb pain paraesthesia, & weakness Urine retention MRI findings Fusiform cord swelling (T9, T10) Secondary to ischemia High T2 signal (T6 to conus) Swollen cord from T9 Low cord signal(T11 - T12) Intramedullary syrinx (T4/5 - T7/8) 1stScan: normal Repeat: High T2 posterior dorsal signal to T9 Conus medullary edema Extramedullary haematopoiesis No Yes but no cord compression No No Hb (g/L) 80 132 113 89 Plt (× 109/L) 451 191 474 438 WBC (× 109/L) 12.7 5.1 12.7 7.7 NRBCs (%) 0.39 ND ND 0.5 Transfusion No Yes Yes Yes Last transfusion None − 2 days − 19 days − 20 days Splenectomy No No Yes No Prior thrombosis Yes No No No Other risk factors * No No No No ND = not detected. * Autoimmune markers, active hepatitis C, prothrombotic screen - non contributory. Disclosures: Cappellini: Novartis Pharmaceuticals: Research Funding.

Spinal dural arteriovenous fistulas are abnormal arteriovenous connections on the surface of the dura. They are supplied by branches of intercostal, lumbar, vertebral, middle sacral, or subclavian arteries and rarely by branches of the internal iliac arteries. We present four cases of spinal dural arteriovenous fistulas supplied exclusively by branches of the internal iliac artery in which the clinical and magnetic resonance presentation were not suggestive of this unusual supply. In our experience, internal iliac artery supply was observed in 12.5% of cases of spinal dural arteriovenous fistulas. We recommend that selective internal iliac arteriography be included in the angiographic evaluation of patients suspected of having a spinal dural arteriovenous fistula.

Purpose Neurological complications associated with coarctation of the aorta are generally intracranial. Less familiar, but equally disastrous are the spinal cord complications of this congenital heart lesion. We report on the endovascular treatment of a unique case of a ruptured anterior spinal artery aneurysm caused by a severe, unrepaired, and previously undiagnosed aortic coarctation. Case report/imaging findings A 56-year-old female with a past medical history of chronic hypertension and coronary artery disease, presented with severe, acute neck pain. Physical examination revealed hypertension, fever, a wide pulse pressure, and aortic regurgitation. Neurological examination was within normal limits at the time of presentation. A CT scan revealed an acute subarachnoid hemorrhage with a small amount of blood in the fourth ventricle and a larger amount at the cisterna magna with extension to the C 1 level. CT angiography of the head/neck and spinal MRI/MRA demonstrated an aneurysm ventral to the spinal cord at C 6–7, associated with a markedly dilated anterior spinal artery (ASA). The ASA aneurysm was believed to be the source of the subarachnoid hemorrhage. Additionally, a severe aortic coarctation was identified in the thorax. Multiple dilated intercostal spinal collateral arteries communicating with the ASA were noted bypassing the aortic coarctation. The patient rapidly lost consciousness during the CT angiography (GCS=6) and as a result she was intubated. Transfemoral spinal angiography was attempted, but failed due to an inability to access the ascending aorta across the coarctation. The patient was transferred to our tertiary center for further evaluation and treatment. We attempted a spinal angiogram via right transbrachial approach elucidating the 7 mm ASA aneurysm with a wide neck (4 mm) at the C 7 level, supplied from a hypertrophied branch of the right thyrocervical trunk. The dome of the aneurysm had an irregular morphology and a daughter sac suggestive of recent rupture. However, endovascular therapy was delayed due to the significant contrast exposure and development of contrast induced nephrotoxicity. Despite our recommendations, aortic coarctation repair was deferred by the cardiothoracic service due to multiple comorbidities. 10 days later, the patient underwent successful endovascular coil embolization of the wide necked ASA aneurysm. Although there was partial encroachment of the parent artery, patent antegrade flow remained secondary to flow demand from this significant collateral route. Summary In the rare cases of spinal artery aneurysms, caused by the high-flow collaterals bypassing an aortic coarctation, correction of the aortic coarctation will usually lead to regression of these aneurysms. However, in our case, the ASA aneurysm had ruptured resulting in cord compression and progressive myelopathy with risk for re-rupture and devastating complications. A multidisciplinary approach is required to address the multi-faceted treatment plan in these complex presentations including aortic coarctation repair, securing the spinal artery aneurysm via endovascular/microsurgical approach, and balancing the hemodynamics of renal perfusion versus aneurysm stabilization. Competing interests None.

We observed spinal vessels ill 150 patients using, routine abdominal CT. Contiguous 1-cm thick incremental scans were obtained 30–60 s after intrayenous administration of 100 nit non-ionic contrast material (300 mg iodine/ml) at 2–3 ml/s. The area from the superior aspect of the liver to the lower poles of the kidneys was scanned. In 132 88 patients the anterior spinal arteries were visualized as an enhanced clot of the anterior surface of the spinal cord on the contiguous slices. The great radicular arteries arteries of Adamkiewicz were also visualized in 41 (27.3%) patients as an accompanying dot on two to seven contiguous slices, at T10-L2. The importance of the recognition of the normal spinal artery in avoiding misinterpretation, and the potential use of enhanced CT in screening for a variety of vascular diseases, are discussed.

We describe a 27-year-old patient who was admitted to our hospital for a tracheal stenosis caused by an adenocystic carcinoma. A tracheal resection procedure was performed and the head was fixed to the anterior chest wall by two sutures. Postoperatively he became tetraplegic, from which he completely recovered after the sutures were removed. We think that the decreased blood flow in the anterial spinal artery with flexion of the neck in combination with hypotension was the direct cause of this major complication.

The infra-aortic spinal arteries caudal to the aortic bifurcation were studied in 20 perinatal and adult cadavers to determine their import relative to extraforaminal approaches to the lower lumbar discs as well as their probable involvement in certain cases of radiculomedullary ischemia. Analysis of these specimens indicated that, despite considerable variation, the arteries to the L4-L5 and L5-S1 intervertebral foramens generally were not related to the disc dorsolateral zones where lateral surgical approaches are best accomplished. Also, the frequency in which the fourth as well as the fifth lumbar and all sacral segmental vessels were dependent on the posterior division of the hypogastric artery may help explain how spinal cord ischemia could occur in individuals with vulnerable cord vascular patterns and/or spinal arteriopathy after interruption of hypogastric artery blood flow during pelvic operations.

Isolated aneurysms of the spinal artery (not associated with arteriovenous malformations) are exceptionally rare. Fewer than 17 cases have been reported in the literature. We report a case of an isolated spinal artery aneurysm causing acute subarachnoid hemorrhage. Spinal artery aneurysms are contrasted with the more common intracranial aneurysms in terms of presentation and pathogenesis. The various clinical presentations of spinal artery aneurysms are discussed as well. A summary of all reported cases of spinal aneurysms, with and without associated arteriovenous malformations, is listed.

An unusual complication of epidural analgesia used to facilitate postoperative pain relief while mobilizing a patient is presented in this case report. A 65-year-old woman with a history of chronic obstructive pulmonary disease, atherosclerotic cardiovascular disease, chronic renal failure, and degenerative vertebral anatomy underwent resection of the left ureter due to an obstructing tumor. The day following the surgery, mobilization to an armchair was started, followed by a decrease in blood pressure. Soon after, flaccid paralysis was sparing of sensory functions, consistent with anterior spinal artery syndrome, was diagnosed. This complication should be taken into account, especially in patients at risk, when considering epidural analgesia techniques in the postoperative period. Comment by Pedro F. Bejarano, M.D. Fortunately infrequent, the Anterior Spinal Artery Syndrome (ASAS) has been described in the early postoperative period in association with surgery involving the retroperitoneum (specially on the left side), as well as unexpectedly with regional anesthesia procedures (Spinal, Epidural and Celiac Plexus Blocks) in the vicinity of the T6 to L2 “critical zone” of medulary arterial blood flow.1,2 This case highlights the importance of a proper evaluation and prevention when feasible, of combining risk factors (besides type of surgery and anesthetic technique) that may potentiate otherwise subclinical—but certainly prevalent—vascular, circulatory or spinal anatomy aging derangements leading to ASAS. As the authors state in the discussion of this case, it is remarkable the aethiological association with an apparently uncomplicated and retrospectively “preventable” hypotensive episode, whether it be a consequence of a relative hypovolemia, a pharmacological (postanesthetic or not) impairment of baropressor responses, or to an excessive local anesthetic sympathetic blockade. Learning from unexpected negative outcomes in anesthesia makes us more sensible to risk factors that are not specially highlighted in daily practice. In this sense, a case with so multiple patient's risk factors including the diagnosis of spinal stenosis, may had lead to other postop analgesia choices, namely systemic or even sole epidural opioid analgesia (that maybe was not considered here due to the COPD) as has been suggested before.3 Moreover, in the scope of an obstructive coronary disease high-risk patient, a more aggressive treatment to the hypotensive episode including quick return to the recumbent or trendelemburg position limiting the isquemia could have favored this neurological adverse outcome. 1. Hong DK, Lawrence HM: Anterior Spinal Artery Syndrome following total Hip Artroplasty. Anesth Intensive Care. 2001;29:62–66. 2. Hachisuka K, Ogata H, Kohshi K: Postoperative Paraplegia with spinal myoclonus possibly caused by epidural anaesthesia: case report. Paraplegia. 1991 Feb;29(2):131–136. 3. Linz SM, Charbonnet C, Mikhail MS, et al.: Spinal artery syndrome masked by postoperative epidural analgesia. Can J Anaesth. 1997;44(11):1178–1181.

To the Editor: In the July 2000 issue of Physical Therapy , Mautes et al, in an article titled “Vascular Events After Spinal Cord Injury: Contribution to Secondary Pathogenesis,”1 described the blood supply to the spinal cord. The authors stated that a segmental spinal artery enters the intervertebral foramen and divides into 3 branches outside the spinal canal at each segmental level of the spinal cord: the anterior and posterior longitudinal spinal canal arteries and the radicular artery. Furthermore, Mautes et al described the radicular artery continuing along the nerve root and dividing into an anterior radicular artery and a posterior radicular artery. They stated that, after penetrating the dura mater, the anterior and posterior radicular arteries join the 3 major arteries on the surface of the spinal cord to provide the blood supply to those areas. Mautes et al cited references by Crock and Yoshizawa2 and Domisse3 in their description of the extrinsic blood supply to the spinal cord. Although Mautes and colleagues' description of anterior and …

A 35 year old man experienced severe transitory neck pain following a violent sneeze. This was followed by neurological symptoms and signs indicating a left sided upper cervical cord lesion. MRI showed an infarct at this site in the territory of the left posterior spinal artery. This discrete infarct was probably due to partial left vertebral artery dissection secondary to sneezing.

Epidural or intrathecal infusions of morphine and bupivacaine mixtures are presently used for the treatment of "refractory" cancer pain even though the neurotoxic potential of such mixtures is unknown. The pathologic findings of the spinal column, the meninges, the nerve roots, and the spinal cord, and the clinical neurologic deficits were recorded in 15 patients (5 men and 10 women), aged 26-83 (median 68) yr, treated for 4-274 (median 81) days with intrathecal infusions of morphine (with preservatives [sodium metabisulfite and sodium edetate]) and bupivacaine mixtures, given through open, subcutaneously tunneled nylon catheters. Six patients had been subjected to radiation therapy (20-96 Gy), applied over the spinal column, and four had been treated with antineoplastics believed to be neurotoxic. Ten patients had various neurologic deficits before the intrathecal treatment. The cumulative doses (ranges) given intrathecally were: morphine 33-11,900 mg, sodium metabisulfite 3.3-1,050 mg, sodium edetate 0.33-105 mg, and bupivacaine 10-41,400 mg; cumulative volumes were 16-9,400 ml. The concentrations of the drugs in the mixtures were: morphine 0.25-4.0 mg/ml, sodium metabisulfite 0.025-0.40 mg/ml, sodium edetate 0.0025-0.04 mg/ml, and bupivacaine 3.0-4.75 mg/ml. The osmolality of the mixtures in vitro ranged from 282 to 286 mOsm/kg and the pH from 4.1 to 4.6. The pathologic findings consisted of vertebral metastases (n = 6), epidural and/or intrathecal tumor masses (n = 8), focal subdural fibrosis (n = 6), infiltration of mononuclear cells in the subarachnoid space (n = 10), and discrete injuries (nerve fiber degeneration or fibrosis) to the anterior (five patients) and posterior (seven) nerve roots, and spinal cord (tumor compression [one], slight thickening of the leptomeninges [one], and thrombosis of a spinal artery and medullary infarction [one]). In none of the cases was any reaction against the nylon catheter within its subarachnoid course recorded. The neuropathologic findings were not related to the duration or cumulative doses of the intrathecal treatment. No new neurologic deficits that could be attributed to the intrathecal administration of the opiate-bupivacaine mixtures were recorded. The neuropathologic and clinical neurologic findings in cancer patients treated with intrathecal morphine-bupivacaine mixtures appeared similar to those in animals and humans reported with either intrathecal morphine or bupivacaine alone.

✓ The case of a 57-year-old woman with a 14-year history of progressive paraparesis is presented. Selective spinal angiography revealed a juvenile-type spinal arteriovenous malformation (AVM) with a typical large size and rapid flow. The AVM was located primarily in the retromedullary space at the cervicothoracic junction. The AVM was successfully obliterated by intraoperative embolization using isobutyl-2-cyanoacrylate and surgical excision.

rapidly by complete tetraplegia. On presentation he had no lowerextremity motor function and a T-11 sensory level (American Spinal Injury Association [ASIA] Grade A; ASIA motor score 50). A small bowel obstruction had been diagnosed 1 week prior to presentation, and he had undergone a laparotomy and lysis of adhesions for similar pain; there had been no other features of a bowel obstruction. The patient’s medical history was significant for hypertension. His surgical history was significant for having undergone an open cholecystectomy for cholecystitis 15 years prior to the current event. There was no history of connective-tissue disorders in the patient or his family. Spinal magnetic resonance (MR) imaging demonstrated a subdural and intramedullary hemorrhage in the lower thoracic spine (Fig. 1A). Spinal angiography revealed an aneurysm arising from the posterior spinal artery at T-12 (Fig. 1B). Surgical exploration confirmed the subdural hematoma and an area of hemorrhage within the left posterior aspect of the spinal cord, and the fusiform aneurysm was identified in the hemorrhage cavity (Fig. 1C). The aneurysm was resected. Histopathological analysis revealed a disrupted elastic lamina and organized thrombus in the media and adventitia, consistent with an arterial dissection (Fig. 2). At the 2-month follow-up examination the patient had minimal improvement in function—specifically, only subjective improvements in sensation and no change in sensory level, motor score, or ASIA grade. Intraspinal aneurysms are rare lesions and have been identified in association with arteriovenous malformations and vessels collateralizing around a thrombosed vessel,1–3 suggesting that they may form as a result of high-flow states in the vessel of origin. The most common vessel of origin is the anterior spinal artery, and the most common region of involvement is the cervicomedullary region.1,4 This case is unique in that the aneurysm arose from the thoracic posterior spinal artery and it was secondary to a dissection. Several features suggest a dissection as the cause. These include the history of hypertension, at least two episodes of acute severe abdominal pain, the fusiform nature of the aneurysm, and the histological features of the lesion.

Ischemic spinal cord injury is a serious complication after surgical repair of descending thoracic or thoracoabdominal aortic aneurysm. The Adamkiewicz artery (arteria radicularis magna [ARM]) is well known as a main feeder of the spinal cord. It originates from a segment of the intercostal or lumbar artery. The anatomical information of the ARM is important in conducting surgical strategy and may reduce the risk of postoperative neurologic deficit. To detect the ARM, selective angiography and magnetic resonance angiography have been used and reported to identify the ARM in 70% to 80% of patients. Alternatively, we have adopted a fourchannel multi-detector row computed tomographic (MDCT) scan that could successfully visualize the ARM. A 70-year-old man with a dissecting thoracoabdominal aortic aneurysm (DeBakey type IIIb; maximal diameter, 60 mm) underwent MDCT scan, as seen in this helical computed tomographic image (Fig 1A). The axial computed tomographic image shows the aneurysm that it is 60 mm in maximal diameter (Fig 1B). The study revealed the ARM originating from the left L1 lumbar artery and connecting to the anterior spinal artery with the classic “hairpin” bend, as seen in this preoperative MDCT scan with coronal reformation (Fig 2 [ASA aspirin]). His surgical repair consisted of aneurysmectomy and graft replacement with the reconstruction of the left T8 and T10 intercostal arteries, the left L1 lumbar artery, the celiac artery, the superior mesenteric artery, and the bilateral renal arteries. To minimize the duration of spinal cord ischemia, the left L1 lumbar artery was reconstructed first. The postoperative MDCT scan after the operation showed that the ARM was successfully reconstructed (Fig 3) and no neurologic complication was noticed. The MDCT scan was acquired under a protocol approved by our institutional review board. Computed tomographic images were obtained while injecting 100 mL of 350 mg/dL iodinated contrast medium at a flow rate of 5 mL per second through the right antecubital vein. A 0.5 second tube-detectors rotation time and helical pitch 5 were used. The patient was requested to breathe quietly during the scan. All computed tomographic data were processed in our three-dimensional imaging workstation to get sagittal and coronal reformations of 1-mm thickness. The MDCT scan is noninvasive to visualize the ARM and helpful in surgical repair of the descending thoracic or thoracoabdominal aortic aneurysm. Moreover, this study is economically acceptable and is not time consuming. Address reprint requests to Dr Shiiya, Department of Cardiovascular Surgery, Hokkaido University School of Medicine, Kita 14, Nishi 5, Kita-ku, Sapporo, Hokkaido 060-8648, Japan; e-mail: shiyanor@ med.hokudai.ac.jp. Fig 1.

A case of an anterior cervical spinal artery originating from a right vertebral artery with a bifid origin is presented. Such an origin may have important surgical consequences, and must be evokated when the vertebral artery enters the cervical canal at an unusual level.

Three patients paraplegic following anterior spinal fusion for congenital kyphoscoliosis were noted to have complete somatosensory evoked potential signal loss shortly after segmental arterial ligations at the apex of their respective kyphosis. This has prompted us to use temporary segmental arterial occlusion with somatosensory evoked potential monitoring prior to ligation during anterior spinal fusion. As a result, we have noted seven additional cases, out of a total of 44 cases monitored in this fashion, in which complete loss of somatosensory evoked potential signals, reversible by release of vascular clips, has occurred. For each of these additional cases the critical segmental arteries were identified and were not ligated, usually resulting in some modifications in the planned surgical procedure, and the patients remained neurologically intact. We recommend temporary segmental arterial occlusion with somatosensory evoked potential monitoring during thoracolumbar anterior spinal fusion to potentially avert ischemic neurologic injury. Based on published data and the experience described herein, this technique should be especially important in anterior spinal fusion for congenital kyphoscoliosis.

Spinal cord infarction in the region of the posterior spinal arteries is reported in a 62-year-old woman. The softening was restricted to the lumbosacral region involving two segments. Sectioning the affected and adjacent segments serially no occlusion was found in the posterior spinal arteries. Besides the circumscribed infarction the microscopic picture of the spinal cord was characteristic of vascular myelopathy. The underlying disorders of the previously reported cases and the predisposing factors contributing to the development of infarction are discussed. It is concluded that an insufficient anastomotic network plays the essential role in the pathogenesis of the spinal cord infarction.

An intraspinal vascular malformation associated with the Klippel-Trenaunay-Weber (KTW) syndrome initially was thought to be intramedullary on angiographic findings. Postmortem examination revealed an entirely posterior extramedullary arteriovenous fistula (AVF) fed by the anterior spinal artery. The association of the KTW syndrome with a so-called intramedullary AVF has been described in the literature without any pathologic confirmation (11 cases). Our case emphasizes the difficulty of determining the exact morphology and location of spinal AVF on arteriography. The association of the KTW syndrome with a retromedullary AVF can be explained on a developmental basis.

Spinal cord ischemia following operations on the abdominal aorta is considered an unpredictable event attributable to variations in spinal cord blood supply. Our experience with seven cases of spinal cord ischemia contradicts this hypothesis. All patients had a bifurcation graft implanted. Three patients had bilateral interruption of hypogastric circulation. Each had gluteal necrosis and two had left colon ischemia. Two patients had unilateral hypogastric ligation. In both of these patients, early postoperative hypotension preceded recognition of spinal cord ischemia. Two patients without known interruption of hypogastric flow had proximal side-to-end anastomoses placed in an atheromatous aorta. Intraoperative peripheral emboli occurred in one and postoperative visceral emboli occurred in the other patient. In the latter case spinal cord ischemia occurred late concomitantly with embolization. The surmised important details in patients' courses with spinal cord ischemia are (1) interference with pelvic blood flow (five of seven patients) severe enough in three cases to cause gluteal necrosis and (2) a high incidence of perioperative complications. Interruption of an anomalous spinal artery was probably not a factor as cord lesions were mostly distal and no case of spinal cord ischemia occurred after a cylinder graft was placed. Spinal cord ischemia is potentially preventable. Our experience reemphasizes the importance of hypogastric perfusion, the dangers of handling the atheromatous aorta, and the necessity for avoiding postoperative hypotension. (J VASC SURG 1986;3:94-103.)

A rich serotoninergic innervation of the anterior spinal artery has been evidenced by histofluorescence. The main contribution to this adventitial serotoninergic plexus appears to originate from a serotonin fiber network in the anterior horns: serotonin-containing fibers reach the dorsal termination of the sulcocommissural artery and run within its wall in a ventral direction, toward the anterior spinal artery. This segmental arrangement of blood vessel innervation could be the basis for a neurogenic control of local blood circulation.

This study was designed to extend our present knowledge of the origin and distribution of anterior spinal arteries and was carried our using 31 human cadavers with arterial injections of natural latex. The conclusions reached are that there are always one or two anterior spinal arteries (right or left) which proceed from the intracranial segment of the vertebral arteries. These arteries have a descending course, with distribution into the ventral face of the medulla oblongata and the first cervical segments of the medulla spinalis. In cases where there are two anterior spinal arteries, they anastomose with each other to form the common, unpaired and median anterior spinal artery. The different observed locations of the origins of anterior spinal arteries m ay be systematised into three types. Each of these types has differential characteristics: bilateral origin (type I; 77.4%), unilateral origin (type II; 9.7%) and origin in an intervertebral transversal anastomosis (type III; 12.9%). We do however subdivide the bilateral origin group, according to the calibre of the arteries, into the subtypes ‘balanced’ (type la; 22.6%), ‘right dominated’ (type lb; 32.2%) and ‘left dominated’ (type Ic; 22.6%). The collaterals of the anterior spinal arteries which distribute into the ventral face of the medulla oblongata are described.