Anterior Spinal Artery Syndrome: Rare Precedented Reason of Postoperative Plegia After Spinal Deformity Surgery: Report of 2 Cases.

BACKGROUND: Complications in spinal deformity surgery vary from insignificant to severe. Apart from direct mechanical insult, ischemia can also cause spinal cord injury. Ischemic injury may be detected during surgery or may manifest itself postoperatively. We present 2 cases of anterior spinal artery syndrome. CASE DESCRIPTION: In the first case, a 12-year-old girl developed anterior spinal artery syndrome resulting in total quadriplegia 8 hours after spinal deformity surgery. She was treated with a steroid, immunoglobulin, and low-molecular-weight heparin. She showed complete recovery at 1 year postoperatively both clinically and radiographically. In the second case, a 62-year-old woman experienced sudden loss of motor evoked potentials intraoperatively during dural tear repair after sagittal and coronal alignment was established. The paraplegic patient was diagnosed with anterior spinal artery syndrome at the thoracic level postoperatively. She was treated with a steroid and heparin. At 1 year postoperatively, she has gained much of her strength and has myelomalacia in her spinal cord. CONCLUSIONS: Anterior spinal artery syndrome is a serious condition with a generally poor prognosis. Though treatment should be directed at the underlying cause, the best strategy is to prevent it from occurring. Peroperative blood pressure control, intraoperative neuromonitoring, avoidance from mechanical stress during surgery, and close neurologic and hemodynamic monitorization postoperatively should be performed.

A case of anterior spinal cord syndrome in a patient with unruptured thoracic aortic aneurysm with a mural thrombus.

BACKGROUND: Spinal cord infarction is an uncommon condition. Anterior cord syndrome present with paraparesis or quadriparesis with sparing of vibration and proprioceptive senses. The common causes of anterior cord syndrome are aortic dissection and aortic surgical interventions. Spontaneous unruptured nondissected aortic aneurysms with intramural thrombus can rarely cause anterior cord infarctions. CASE PRESENTATION: We report a case of anterior spinal cord syndrome due to aneurysm of the thoracic aorta with a mural thrombus. A 64 year old male presented with sudden onset paraparesis with a sensory level at T1 with preserved sense of proprioception and vibration. The MRI panspine revealed increased T2 intensity in the anterior portion of the spinal cord from C5 to T10 level with characteristic 'owl eye' appearance on axial imaging. The CT aortogram detected aneurysmal dilatation of the ascending aortic, arch and descending thoracic aorta with significant intimal irregularities, calcified atherosclerotic plaques and a small mural thrombus. CONCLUSION: The possible mechanisms postulated are occlusion of ostia of radicular arteries by the atherosclerotic plaques and mural thrombus or thromboembolism to the anterior spinal artery. Nondissected atherosclerotic aortic aneurysms should be considered in patients presenting with spinal cord infarctions especially in the presence of vascular risk factors and smoking.

Spinal cord infarction post cardiac arrest in STEMI: A potential complication of intra-aortic balloon pump use.

Intra-aortic balloon pump (IABP) is commonly used as a cardiac assist device in various clinical situations: cardiogenic shock, mechanical complications of acute myocardial infarction, high risk percutaneous coronary interventions, coronary artery bypass graft surgery and refractory unstable angina and ventricular arrhythmias as bridge to therapy. Although current data support its safety, there is limited or no support for its efficacy. We present the case of spinal cord infarction after IABP use in a patient who presented with ST elevation myocardial infarction and cardiac arrest and we discuss the potential mechanism of such a devastating complication.

Anterior disco-osteo-arterial conflict as a cause of intersegmental arterial flow impairment and spinal cord ischemia.

INTRODUCTION: This article describes anterior disco-osteo-arterial conflict as an insofar unsuspected mechanism of arterial flow impairment potentially leading to spinal cord ischemia and infarction. METHODS: The anterior disco-osteo-arterial conflict described in this report is illustrated with angiographic observations of patients presenting with spinal cord ischemia documented by MRI, and radiculomedullary flow impairment diagnosed by spinal digital subtraction angiography and spinal CTA. RESULTS: Proximal intersegmental artery flow impairment was found in association with anterior disc bulging and anterior osteophytic formation, alone or in combination. Patients either presented with an initial acute medullary syndrome or with a long-standing history of spinal claudication with acute secondary pejoration. CONCLUSION: Spinal ischemia can be the result of intersegmental and radiculomedullary flow impairment caused by an anterior disco-osteo-arterial conflict.

Thoracic disc herniation leads to anterior spinal artery syndrome demonstrated by diffusion-weighted magnetic resonance imaging (DWI): a case report and literature review.

BACKGROUND: Thoracic disc herniation rarely causes acute ischemic events involving the spinal cord. Few reports have suggested this as a mechanism leading to anterior spinal artery syndrome, and none with illustration through diffusion-weighted magnetic resonance imaging (DWI). PURPOSE: The purpose of this study was to report a case of anterior spinal artery syndrome secondary to thoracic disc herniation and demonstrate the first use of DWI to aid in diagnosis of this rare myelopathy. STUDY DESIGN: Case report. METHODS: A 36-year-old woman developed sudden onset of back pain followed by evolving paraparesis and sensory loss consistent with anterior spinal artery distribution ischemia. T2-weighted magnetic resonance imaging (MRI) demonstrated an acute herniated nucleus pulposus at the T7-T8 disc, which produced a focal indentation of the adjacent anterior spinal cord without cord displacement or canal stenosis. T2-weighted hyperintensities were seen at T4-T7 levels with corresponding brightness on DWI and reduction of the apparent diffusion coefficient, consistent with cord ischemia. RESULTS: Remarkably, within just a few days and following conservative treatment, including heparin and steroids, this patient's neurologic status began to show improvement. Within 3 weeks, she was ambulating with assisted devices, and at the 10-month follow-up, the patient had nearly complete neurological improvement. A follow-up MRI at 10 months showed normal T2-weighted imaging except for a 1×2-mm area of anterior-left lateral cord myelomalacia at T4-T5. CONCLUSIONS: Acute thoracic disc herniation with cord contact but without canal stenosis is able to disrupt blood flow to the cord leading to anterior spinal artery distribution ischemia. This case represents the first demonstrated use of DWI in diagnosing this rare cause of anterior spinal artery ischemia.

Complex arteriovenous fistulas at C1 causing hematomyelia through aneurysmal rupture of a feeder from the anterior spinal artery.

A 64-year-old woman presented with left occipital headache and right dissociated sensory loss due to hematomyelia on the left ventral side of C1 caused by rupture of an aneurysm on one of the feeders extending from the anterior spinal artery to complex epidural or dural and intradural arteriovenous fistulas (AVFs). Branches from the left occipital and ascending pharyngeal arteries and those from the left C2 radicular, left posterior spinal and anterior spinal arteries formed these multiple shunts, linking with a common venous drain flowing into the right petrosal vein. Surgical interception of all the shunts was achieved, making it unnecessary to directly treat the aneurysm in the spinal cord. The feeders, aneurysm and AVFs were not visualized on postoperative angiography, and the patient returned to a normal working life.

Role of degenerated neuron density of dorsal root ganglion on anterior spinal artery vasospasm in subarachnoid hemorrhage: experimental study.

BACKGROUND: The spinal arteries are innervated by several systems that contribute to the control of spinal cord blood flow. The sensory fibers of upper cervical nerves have vasodilatatory effect on the anterior spinal arteries (ASA). Subarachnoid hemorrhage (SAH) causes severe vasospasm by various neurochemical mechanisms. We examined whether there is a relationship between the neuron density of the C3 dorsal root ganglion and the severity of ASA vasospasm in SAH. METHODS: This study was conducted on 20 rabbits. Four of them were used as baseline group. Experimental SAH has been applied to all of 16 animals by injecting homologous blood into cisterna magna. After 20 days of injection, ASA and C3 dorsal root ganglia (C3DRG) were examined histopathologically. ASA volume values and normal and degenerated neuron densities of C3DRG were estimated stereologically and the results were analyzed statistically. RESULTS: The mean ASA volume was 1.050±0.450 mm³, [corrected] and the mean neuronal density of C3DRG was 10,500 ± 850 in all animals. The mean volume value of ASA was 0.970±0.150 [corrected] mm³, and the normal neuron density of C3DRG fell to 8,600 ± 400/mm³ in slight vasospasm group. In severe vasospasm-developed animals, mean volume value of ASA was 0.540±0.90 [corrected]mm³ and the normal neuron density of C3DRG fell to 5,500 ± 360/mm³. An inverse relationship between the degenerated neuronal density of the C3DRG and ASA volume values may indicate the severity of ASA vasospasm. CONCLUSION: The neuron density of C3DRG may be an important factor on the regulation of ASA volume values and the continuation of spinal cord blood flow. Low neuron density of C3DRG may be considered as an important factor in the pathogenesis of severe ASA vasospasm in SAH.

Anterior spinal artery syndrome in a 16-year-old male.

Spinal cord infarction is a relatively uncommon condition in young children and adolescents, however, it should be included in the differential diagnosis of acute cord compression. Depending on the vessel involved, the clinical presentation may differ. The degree of recovery in spinal cord infarcts varies from one individual to another. Recovery of motor function is progressive in most of the patients, with the deficit being maximal at the onset. For successful outcome, it is imperative that these patients get access to approriate rehabilitation very early in the course of the disease. Prevention and early treatment of specific complications, especially chronic pain, is of vital importance in young patients. This article describes our experiences diagnosing and treating a 16-year-old boy with anterior spinal artery syndrome.

Post-traumatic cervical kyphosis with surgical correction complicated by temporary anterior spinal artery syndrome.

Post-traumatic undiagnosed disco-ligamentous and osseous lesions of the cervical spine may eventually result in irreducible extreme kyphosis. Correction of such consolidated deformities requires major surgery with a combined posterior and anterior approach, aiming to correct bony impingement on neural and vascular structures, reduce deformity and to attain circumferential instrumentation and fusion in physiological alignment. This can be achieved using either a single-staged or a two-staged procedure. Regardless, this type of major surgery entails considerable neurological risks. Therefore, thorough planning of the intervention and considerable surgical experience is needed. We present an elderly woman with gross restriction of forward gaze and intractable nuchal and radicular pain due to cervical spine deformity. Her cervical kyphosis was corrected using preoperative skeletal axial traction for four days and subsequent operative reduction with circumferential instrumentation and fusion. The post-operative course was complicated by a temporary anterior spinal artery syndrome despite normal intraoperative somatosensory evoked potentials (SSEP) and by a wound infection requiring removal of the implant. Nevertheless, segmental fusion in physiological alignment was successfully achieved and the patient fully recovered from the neurological deficit and infection. Quality of life was significantly improved.

[A neonatal case of anterior spinal artery syndrome presenting with bilateral arm paresis].

Anterior spinal artery syndrome is rare in children, especially in neonates. We present a girl with hydrops fetalis and hypothyroidism who developed flaccid paresis of both arms in the neonatal period (around day 25). MRI of the spine performed on day 52 revealed atrophic changes at C5-Th1 without Gd-DTPA-induced enhancement. Nerve conduction studies were also helpful in the diagnosis;in the upper limbs, motor potential was not elicited, while sensory nerve conduction velocity was normal. These clinical and laboratory findings suggested an atypical case of anterior spinal artery syndrome.

Blood distribution to the anterior spinal artery from each segment of intercostal and lumbar arteries.

AIM: Prevention of paraplegia, a serious complication of surgery for thoracoabdominal aortic aneurysm, has been well documented. However no assured prophylaxis against this complication has yet been found. Spinal ischemia is believed to be the major cause of paraplegia. We conducted an experimental study to define the development of paraplegia with regard to the blood supply to the spinal cord. METHODS: A porcine model was used to evaluate blood distribution to the anterior spinal artery. Colored silastic agent was selectively injected into the intercostal and lumbar arteries, and distribution to the anterior spinal artery was evaluated on 50 animals. The intercostal and lumbar arteries were ligated in the segments where the blood supply to the anterior spinal artery would be interrupted. Whether or not paraplegia developed was checked 2 days later. RESULTS: Colored silastic agent arrived at the anterior spinal artery from all segments of the 8th intercostal to 4th lumbar arteries. Two of 9 pigs (22.2%) that underwent ligation of the segments from the 9th intercostal to 2(nd) lumbar artery suffered paraplegia. In 3 non-paraplegic pigs, colored silastic agent injected into the preserved arteries was found to have covered a wider range. CONCLUSION: All the intercostal and lumbar arteries supplied blood to the anterior spinal artery. When large segments of intercostal and lumbar arteries were ligated, the blood flow from the preserved segments acquired increased dominance. The possibility exists that any intercostal and lumbar artery can supply blood to the spinal cord and become collateral circulation to the anterior spinal artery.

Anterior spinal artery syndrome after aortic surgery in a child.

Anterior spinal artery syndrome is rare in children. In adults, where it is observed most frequently after resection of thoracoabdominal aortic aneurysms, spinal magnetic resonance imaging is considered the first-line investigation to confirm the clinical diagnosis. A 3-year-old male who presented with this syndrome after palliative cardiac surgery for a complex cardiac malformation associated with aortic coarctation is presented. Clinical diagnosis of anterior horn cell impairment below the L2 level was confirmed by electromyography and F-wave studies. Sparing of dorsal sensory tracts was documented by normal somatosensory-evoked potentials, which confirmed the anterior localization of the lesion. Spinal magnetic resonance imaging performed on day 15 and day 105 after surgery was normal. Neurologic deficits, including flaccid paraplegia, remained stable except for the reappearance of patellar reflexes on day 83. Neurophysiologic conduction studies were consistent with lower motoneuron loss. In this patient, magnetic resonance imaging was less sensitive in demonstrating spinal cord lesion than clinical neurophysiology. Somatosensory-evoked potentials failed to detect the insult. Prevention may therefore require other neurophysiologic monitoring techniques.

Anterior spinal artery syndrome in an adolescent with protein S deficiency.

The diagnosis of anterior spinal artery syndrome can be made with high accuracy by thorough clinical examination in combination with typical magnetic resonance imaging findings. Sudden onset of tetra- or paraparesis and dissociated sensory loss with bladder dysfunction are the leading clinical signs. We discuss clinical and radiologic findings in an adolescent presenting with anterior spinal artery syndrome. The laboratory results showed a hereditary protein S deficiency.

The crossing of the spinothalamic tract.

The question whether the spinothalamic and spinoreticular fibres cross the cord transversely or diagonally was investigated in cases of anterolateral cordotomy and in a case of thrombosis of the anterior spinal artery. The pattern of sensory loss following transection of the anterolateral quadrant of the cord consists of a narrow area of decreased nociception and thermanalgesia at the level of the incision; it extends for 1-2 segments cranial and cordal to the incision. This area is immediately cranial to the area of total loss of these modalities. This pattern of sensory loss is explained as follows. The cordotomy incision transects two groups of fibres: those that are already within the anterior and anterolateral funiculi and those that are crossing the cord. The area of total thermanaesthesia and analgesia is due to transection of fibres that are already within this region. The area of partial sensory loss is due to transection of the fibres that are crossing the cord at that level. Owing to the craniocaudal extent of the branches of the dorsal roots, there is an overlap of their collaterals that results in every spinothalamic neurone receiving an input from several dorsal roots. The narrow cordotomy incision thus divides the few fibres crossing at that level, causing diminished noxious and thermal sensibility over a few segments above and below the incision. These facts can be accounted for only on the assumption that these spinothalamic fibres are crossing the cord transversely. This evidence of transverse crossing was found in the cervical, thoracic and lumbar segments. There were three of 63 cordotomies for which this explanation of the partial sensory loss could not be maintained. Although no explanation has been suggested, this is unlikely to be due to the fibres crossing the cord diagonally.