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Herein, we described 2 patients with posterior spinal artery syndrome (PSAS) caused by vertebral artery dissection. The patients complained of sudden neck pain or walking instability. Neurological examination revealed sensory loss, muscle weakness, and sensory ataxia. Angiography showed double lumen sign or intimal flap in the vertebral artery. T2-weighted imaging and diffusion-weighted imaging of MRI showed a hyperintense lesion in the dorsal side of the cervical spinal cord at different times after onset. Both patients had good outcome after antiplatelet therapy and physiotherapy. A review of previously reported PSAS cases was also conducted in order to improve the understanding and awareness of this rare myelopathy., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Chronic subdural hematoma (CSDH) is uncommon in the spine. Most spinal CSDHs occur as solitary lesions in the lumbosacral region. We report a rare case of multiple spinal CSDHs associated with hematomyelia. The diagnostic and therapeutic management of these complex spinal CSDHs is reviewed as well as the pertinent literature., Case Description: A 79-year-old woman on warfarin therapy presented with lower back pain and progressive lower extremity weakness that had developed in the previous 2 weeks. She subsequently developed paraplegia and urinary incontinence. Thoracolumbar magnetic resonance imaging showed a CSDH from T12-L3 compressing the cauda equina. Single-shot whole-spine magnetic resonance imaging showed another CSDH and hematomyelia at T2-3. She underwent L2-3 hemilaminectomy, which revealed a liquefied subdural hematoma. Delayed T2 laminectomy exposed an organized subdural hematoma and xanthochromic hematomyelia. After each surgery, the patient showed significant motor recovery. Finally, the patient could walk, and the urinary catheter was removed., Conclusions: Spinal CSDH may occur in multiple regions and may be associated with hematomyelia. Whole-spine magnetic resonance imaging is useful to examine the entire spine for CSDH accurately and thoroughly. Comprehensive surgical exploration of all symptomatic hematomas may restore neurologic functions even with delayed surgery., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Hemorrhagic presentations are rare in vertebrovertebral arteriovenous fistula (VVAVF). To the best of our knowledge, this is the first report of a patient initially presenting with subarachnoid hemorrhage and progressing to intramedullary hemorrhage., Case Description: The authors report on a 59-year-old man with VVAVF who developed massive intramedullary hemorrhage. Twelve months before ictus, the patient presented with subarachnoid hemorrhage. Although we recommended endovascular surgery, the patient refused treatment. Twelve months after the initial attack, the massive intramedullary hemorrhage in cervical spinal cord caused complete spinal cord injury. Emergent endovascular intervention was performed after the intramedullary hemorrhage, but there was no neurologic improvement., Conclusions: Identification of this phenomenon is important in VVAVF because intramedullary hemorrhage dramatically degrades patient outcome. Prompt surgical intervention is mandatory for VVAVF cases presenting with subarachnoid hemorrhage., (Copyright © 2019. Published by Elsevier Inc.)

Spinal subarachnoid hemorrhage (SAH) is a rare disease. Spinal aneurysms are even rarer and mostly undetected unless they rupture and become symptomatic. In this chapter we aim to review the available literature about spinal subarachnoid hematoma with special emphasis on spinal aneurysms. As most reports of spinal aneurysms describe a single case or a small case series, the diagnostic algorithm is often lacking. The outcome is also different based on the etiologies; therefore management strategy must be individualized. We addressed these issues in this chapter. The reported incidence of spinal SAH is less than epidural hematoma and more than subdural hematoma. Spinal aneurysms can present as isolated entity or can be associated with other vascular anomalies. Microsurgical clipping and/or resection is possible, especially when they are located dorsally or dorsolaterally. Endovascular approach is also a feasible option unless negotiation of microcatheter becomes difficult in tortuous small-caliber arteries. Successful obliteration leads to good outcome, especially when present in posterior spinal artery. A detailed knowledge of spinal SAH and spinal aneurysms is important to detect them in time. Clinicians must consider several factors to choose an appropriate treatment strategy to ensure the safety of their patients., (© 2017 Elsevier B.V. All rights reserved.)

Background: Spontaneous or idiopathic intramedullary bleeding is a very rare event in pediatric patients. This diagnosis requires an extended clinical, laboratory, and radiologic work-up to rule out all potential causes of hematomyelia. However, children may present with hematomyelia or spinal cord injury without radiographic abnormality even after a minor trauma., Case Description: A 15-month-old girl presented with a 24-hour history of progressive neurologic deficits. A trivial trauma had occurred a few days before the clinical onset. Head computed tomography scan and craniospinal magnetic resonance imaging revealed an isolated hemorrhagic central medullary lesion extending from the obex to C3 level. No underlying causes of intramedullary bleeding were identified. In the absence of obvious vascular abnormalities, the patient underwent an urgent occipitocervical decompression with hematoma evacuation. Postoperatively, the patient's motor symptoms rapidly resolved, and she was discharged with cervical collar immobilization., Conclusions: We discuss the differential diagnosis of intramedullary bleeding in children, focusing on the diagnostic protocol and therapeutic options in this age group., (Copyright © 2016 Elsevier Inc. All rights reserved.)

We report a case of left upper cervical posterior spinal artery (PSA) syndrome caused by atherosclerosis of the left vertebral artery. A 70-year-old female experienced sudden dizziness and paralysis of the left upper and lower limbs. Diffusion-weighted magnetic resonance imaging (DWI) of the brain showed high signal intensity at the vermis and lower left hemisphere of the cerebellum, and magnetic resonance angiography showed that the entire left vertebral artery was thin. The patient was treated with an intravenous infusion of tissue plasminogen activator 2 hours after symptom onset and made a full recovery. Repeat DWI, fluid-attenuated inversion recovery images, and T2-weighted images showed high signal intensity in the left upper cervical PSA area from the lower medulla oblongata to the C2 level in addition to the cerebellum. Previously reported cases of cervical posterior artery syndrome are reviewed., (Copyright © 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Perimedullary arteriovenous fistula (AVF) is a relatively rare spinal vascular malformation. Although it has traditionally been considered to be a congenital lesion, some cases identified in adults have suggested that the lesion may be acquired. The etiology and exact mechanism of these lesions are unknown. The authors present a case of a perimedullary AVF caused by a direct stabbing injury of the spinal cord and induced by subsequent kyphosis, and they discuss the pathogenesis and treatment strategy.

Objective: To describe a rare autopsy case of posterior spinal artery syndrome with marked swelling of the spinal cord, an unusually subacute onset and short clinical course., Methods: Case report., Findings: An 84-year-old Japanese woman presented with bilateral muscle weakness of the lower legs and sensory disturbance 1 week after head contusion. Neurological findings worsened gradually. She developed phrenic nerve paralysis and died of respiratory failure 6 weeks after the onset of neurological symptoms. On pathological examination, the spinal cord was markedly swollen in the cervical and upper thoracic segments. Microscopically, there was loss of myelin sheath in the bilateral posterior columns and neuronal loss of the posterior horns in all of the spinal segments. However, findings were unremarkable in the bilateral anterior columns and bilateral anterior horns in most of the spinal segments. Posterior spinal arteries had no stenosis, occlusion, or thrombosis. We considered that pathogenesis was infarction associated with head injury., Conclusion: To our knowledge, this is the first report of a case of posterior spinal artery syndrome with a markedly swollen spinal cord and poor prognosis.

Hematomyelia is rare, and usually related to major trauma. Non-traumatic causes are much rarer and include underlying vascular malformations and cord tumors. We present the case of a previously well 44-year-old woman who developed severe acute neck pain and right-sided motor deficit after a session of traditional Chinese massage that entailed minimal neck manipulation. Emergent MRI confirmed hematomyelia of the right cervical hemicord, notably without associated bony or ligamentous injury. Follow-up spinal angiography and MRIs revealed no underlying vascular malformation or tumor. We highlight this case as there has been no reported case of hematomyelia occurring after mild trauma, although two cases of idiopathic hematomyelia have been reported. Though exceedingly rare, hematomyelia should be considered in the list of differential diagnoses in any case of neck pain and motor deficit after seemingly trivial injury.

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.

We describe a patient with posterior spinal artery (PSA) syndrome due to vertebral artery (VA) dissection. A 63-year-old woman developed neck pain, bilateral shoulder and arm numbness, and paraparesis after prolonged neck extension during a dental procedure. Neurological examination revealed sensory deficits in the legs, paraparesis, cerebellar ataxia, urinary retention and constipation. Magnetic resonance imaging disclosed T2-hyperintense lesions in the posterolateral C4-C7 cord with partial enhancement. T1-hyperintensity and stenosis were found in the right VA at C3-C5. These clinicoradiological findings suggested bilateral PSA syndrome and unilateral VA dissection. This is the fourth report of VA dissection-induced PSA syndrome.

A 44-year-old woman presented with severe headache, drowsy mentality, and right hemiparesis. Brain computed tomography and magnetic resonance angiography revealed non-aneurysmal subarachnoid hemorrhage (SAH). Thoraco-abdominal and pelvic computed tomography angiography showed multiple steno-occlusive lesions involving the aorta and its large branches suggesting Takayasu's arteritis. Spine magnetic resonance imaging was taken because of prominent right hand muscle atrophy on the 14th hospital day, which showed subacute stage of hematomyelia in the cervical cord and conus medullaris. Aneurysmal or non-aneurysmal SAH is rare in patients with Takayasu's arteritis but SAH with coincidental hematomyelia is even more unusual. This case emphasizes the rarity of the coincidental spinal hematomyelia and its importance in the differential diagnosis.

Background/objective: Many atherothrombotic complications are associated with coronary angiography. Spinal cord embolism with high morbidity and mortality is one of these complications., Methods: Case report., Results: A 65-year-old woman was admitted to the hospital with acute myocardial infarction. Immediately after coronary angiography, she complained of paresthesia and paraparesis of her legs. Magnetic resonance imaging (MRI) detected hyperintensity at the level of the conus medullaris. Antiaggregant therapy and a physiotherapy program continued. After 2 months, clinical and MRI findings had improved., Conclusions: Invasive procedures such as coronary angiography can lead to serious atherothrombotic complications.

Hemorrhagic complications in patients with hemophilia have been occasionally reported in the spinal column and the spinal cord. Treatment is based on prompt replacement therapy as the occurrence and development of neurologic dysfunction are related to the length of time between the onset of symptoms and the factor replacement. We report case of a 7-year-old hemophilic boy who presented with flaccid paraparesis resulting from thoracic hematomyelia. The patient showed gradual improvement on medical management with cryoprecipitate infusions. This case calls attention to the need for prompt diagnosis of rarely reported spinal hematomyelia based on clinical manifestations and radiologic features and highlights its management options in patients with hemophilia.

Introduction: Spinal cord hematoma is a serious and feared complication of lumbar puncture. We here describe two patients who developed a spinal cord hematoma following diagnostic lumbar punctures., Case Reports: CASE 1: a 22-year-old male with a syndrome of cerebrospinal fluid hypotension, with normal coagulation parameters, underwent a traumatic, diagnostic lumbar puncture followed, a few hours later, by back pain irradiated to the legs. MRI showed the presence of a subdural hematoma from the lower dorsal region to the sacral region. A conservative approach, without surgery, was decided and he showed a complete recovery. CASE 2: a 69-year-old woman underwent a diagnostic lumbar puncture for the study of recent-onset headache with tinnitus and unstable gait. Puncture was traumatic and cerebrospinal fluid was normal. A few hours later, she complained of back pain and sciatica, and examination revealed a bilateral Lassegue sign. She required urinary catheterization. MRI showed an epidural hematoma from the T10 vertebra to the sacral area. Her outcome with a conservative approach was also excellent., Conclusions: Spinal cord hematomas can occur after a traumatic lumbar puncture in people without coagulation disorders or any other predisposing factor. Although surgery has been traditionally advocated in these cases, a conservative approach is an option when symptoms are mild and a close follow-up is possible.

Background Context: Hemorrhage that results from spinal dural arteriovenous fistula (Type I arteriovenous malformation [AVM]) is uncommon. There are some reports of subarachnoid hemorrhage and subdural hematoma caused by Type I spinal AVM, but there are few reported cases of hematomyelia caused by spinal dural arteriovenous fistula., Purpose: To describe an interesting patient who had hematomyelia caused by a dural arteriovenous fistula (Type I spinal AVM)., Study Design: A case report., Methods: We present a case of a 51-year-old man who presented acute onset epigastric pain, paraplegia, and sensory loss below his nipples. Magnetic resonance imaging and selective spinal angiogram demonstrated hematomyelia, subarachnoid hemorrhage, and spinal arteriovenous fistula fed by the right Th7 intercostal artery. By laminotomy of Th6-8, the varix-like draining vein and intramedurally hematoma were partially removed and the arterial supply was interrupted by coagulation of the right Th7 segmental artery., Results: One month after surgery, he regained movement against gravity at the left ankle and toe but no functionally significant improvement., Conclusions: It must be kept in mind that spinal dural arteriovenous fistulas (Type I spinal AVM) has possibility of hematomyelia origin, despite the fact that it is extremely rare.

Intramedullary spinal cord hemorrhage (hematomyelia) is an uncommon cause of myelopathy and can present in an acute, subacute, stepwise, or chronic fashion. Spinal vascular malformations such as intramedullary cavernomas and intradural arteriovenous malformations are the most common cause of atraumatic intramedullary spinal cord hemorrhage based on the existing literature. Additional considerations include warfarin or heparin anticoagulation, hereditary or acquired bleeding disorders, primary spinal cord tumors, spinal cord metastases, Gowers' intrasyringal hemorrhage, or a delayed complication of spinal radiation. Prompt diagnosis of hematomyelia first requires recognition of a myelopathy syndrome (transverse, central, anterior, posterior, or hemi-cord) often accompanied by sudden, severe back or neck pain and sometimes radicular pain. MRI with and without gadolinium is the preferred imaging modality. There are no clinical trials to guide the management of acute intramedullary spinal cord hemorrhage, and subsequent treatment is usually directed toward the underlying cause.

A 76-year-old woman developed weakness and sensory loss in the lower limbs and urinary disturbance in four days. She had a history of operation for the ascending colon cancer and lung metastasis one year ago. Neurological examination revealed flaccid paraplegia, absent Achilles tendon reflex, severe disturbance of superficial and deep sensation below the L3 level, and vesicorectal abnormality. Magnetic resonance imaging (MRI) studies showed an intramedullary T1-iso, T2-low lesion with Gd-DTPA contrast enhancement in conus medullaris at LI level. The laboratory examination revealed the elevated level of serum FDP. D-dimer and TAT. She was diagnosed as hematomyelia, which may be caused by the activation of coagulation and fibrinolysis system. We suggested that the ascending colon cancer and lung metastasis may contribute to the coagulation-fibrinolysis abnormality.

Introduction: Intramedullary cavernous angiomas (ImCA) of the spinal cord are very uncommon malformations especially in the pediatric population where only ten cases have yet been reported within the available literature., Case Report: In this paper, the authors report the case of a 12-year-old girl presenting with a T11 level hematomyelia because of a cavernous angioma. Microsurgical excision was performed with good clinical outcome and no magnetic resonance imaging evidence of residual cavernoma 30 months later., Discussion: Despite the small number of cases reported in children, this one contributes to the literature identifying special features of presentation and management of ImCA for pediatric patients. Because a higher risk of recurrent bleeding has been demonstrated for ImCA, with dramatic clinical consequences, microsurgical removal remains the only definitive treatment.

Introduction: The prevalence of cerebral cavernomas is about 0.5% in the general population. In contrast, spinal cord cavernomas are considered as rare. The objective of this study was to determine the natural history of spinal cord cavernomas in a multicentric study., Methods: Clinical and neuroradiological findings were retrospectively collected. Diagnosis was based on pathological criteria or magnetic resonance (MR) findings., Results: Fifty-three patients were included (26 males, 27 females). Mean age at onset of symptoms was 40.2 years (range: 11-80). Initial symptoms were progressive (32) and acute myelopathy (20). One patient was asymptomatic. Clinical symptoms were related to spinal cord compression (24) and hematomyelia (19). Cavernoma location was dorsal (41) and cervical (12.). MR findings consisted of hyperintense signal on T1 and T2 sequences (19 cases), mixed hyperintense and hypointense signal (33 cases), and hypointense signal on T1 and T2 sequences in 1 case. Mean size was 16.3 mm (range: 3-54). Forty patients underwent surgical resection. Improvement was observed in 20 patients and worsening of neurological symptoms in 11. Length of follow up was 7.1 years. At the end of the study, 26 patients were autonomous, 18 handicapped and 1 bedridden., Conclusion: This study provided precise data on the clinical and MR patterns of these lesions. The natural history is associated with a higher risk of hemorrhage recurrence, but is favorable in many operated patients. Microsurgery is the treatment of choice for most of these lesions.

A 53-year-old woman presented with a ruptured intramedullary aneurysmal dilatation fed by the anterior spinal artery associated with an arteriovenous malformation located in the ventral cervical spinal cord. She developed tetraparesis and respiratory dysfunction. The neurological deterioration was caused by hematomyelia due to the ruptured aneurysmal dilatation and progression of edema in the upper cervical spinal cord due to venous hypertension associated with additional hematoma in the medulla oblongata. Endovascular embolization of both C-1 and C-2 radicular arteries was performed with Guglielmi detachable coils, but components fed by small branches such as the radiculo-pial artery were not obliterated. Surgery was performed for extirpation of the arteriovenous malformation and cervical intramedullary hematoma, and excision of the aneurysmal dilatation through a transcondylar approach combined with vertebral artery transposition. Postoperatively, she overcame several complications such as pneumonia and endocarditis, and had only moderate weakness of the right upper and lower limbs. This case indicates that surgical intervention for high cervical intramedullary lesion may be very effective.

Study Design: Case report of a patient with subacute delayed myelopathy after an acute low thoracic spine injury., Objectives: To draw awareness to a rarely described complication with potential to add devastating neurological insult to the original spinal cord injury, and to discuss evidence supporting a vascular mechanism., Setting: Health Science Centre, Winnipeg, Manitoba, Canada., Case Report: A 35-year-old woman developed clinical and MRI evidence of ascending myelopathy, extending up to C5, 16 days after a T11/12 fracture dislocation. The distribution of MRI signal abnormality, MRI evidence of prominent venous markings, and association with upright mobilization and the wearing of a thoraco-lumbo-sacral orthosis, suggest that elevated spinal venous pressure in conjunction with low arterial pressure may have induced impaired spinal cord vascular perfusion., Conclusion: After recent spinal cord injury, factors exacerbating spinal venous hypertension and/or arterial hypotension may in some patients lead to impaired spinal cord perfusion. These factors should be considered and corrected if symptoms or signs of progressive myelopathy emerge in the first few days or weeks after injury., (Spinal Cord (2006) 44, 322-325. doi:10.1038/sj.sc.3101801; published online 20 September 2005.)

A 2-year-old male (Hungarian Vizsla) was evaluated for progressive discomfort of possible spinal origin. A minimum data base, thoracolumbar magnetic resonance (MR) imaging examination and electrophysiologic investigation were all normal. Cerebellomedullary and lumbar cerebrospinal fluid (CSF) was collected. The fluid was unremarkable except for elevated total protein. Shortly, thereafter, the dog had progressive neurologic deterioration referable to a caudal lumbar spinal cord lesion. In a repeated MR examination there was a well-circumscribed intramedullary lesion at the site where lumbar CSF was collected. The signal characteristics of the lesion were compatible with subacute hemorrhage, which was confirmed to be hematomyelia at the time of successful decompressive surgery.

We present a case of a reversible spinal venous hypertensive myelopathy that occurred following a traumatic mediastinal hematoma. The mediastinal hematoma caused compression of the brachiocephalic vein, resulting in elevation of the venous pressures that ultimately resulted in dilation of the epidural venous plexus and spinal cord edema. The secondary neurologic deficits were the culmination of venous outflow obstruction at the level of the spinal cord that resolved on the resolution of the mediastinal hematoma.

A 58-year-old man presented with an extremely rare case of "pure type" spinal tanycytic ependymoma associated with hematomyelia manifesting as sensory disturbance of the bilateral hands and weakness of the right arm. Magnetic resonance imaging demonstrated a tumor in the spinal cord from C-2 to C-4 levels. The soft gelatinous tumor was subtotally resected and the adjacent chronic liquid hematoma was aspirated. The immunohistochemical and ultrastructural findings indicated a diagnosis of tanycytic ependymoma.

Objective: To analyse possible relationships between the symptoms and signs created by intradural spinal cord arteriovenous shunts (SCAVSs) and their angio-architecture., Methods: The clinical and radiological files of 155 patients, both adults and children, seen between 1981 and 1999 with a SCAVS were retrospectively reviewed. SCAVSs were divided into nidus type (small superficial or large intramedullary), and fistulas (micro (mAVFs)- or macrofistulas (MAVFs)). The angio-architectural points studied were arterial stenosis, proximal arterial aneurysm, distal arterial aneurysm, arteriovenous fistulas, pial venous drainage and/or reflux, venous ectasias, venous stenosis, venous thrombosis, false aneurysms. Correlations between architecture, location, age groups and symptoms and signs were made., Findings: A male predominance was noted in both adults and children. Most of the lesions were located at the thoracic level, but hemorrhage occurred as the presenting event predominantly in cervical localizations. 30 patients (20 AVMs; 4 mAVFs, 6 MAVFs) were children. 5 of the 6 MAVFs found in children were associated with Hereditary Hemorrhagic Telengiectasia (HHT1). Twenty one children (70%) had bled. Spontaneous total or subtotal recovery was the rule in 15 of those who had bled (72%) but early recurrent hemorrhages occurred in 2. Among 125 adults 56 presented with hemorrhage (45%). The proportions of those who recovered spontaneously (71%) or rebled (3,6%) in the same year after the initial episode were very similar to children. All other adults presented with acute or progressive non-hemorrhagic episodes. There was no significant difference in the angio-architecture between hemorrhagic and non hemorrhagic SCAVS, except for that occurrence of pseudo-aneurysms. Hemorrhage in SCAVSs may not be exclusively due to haemodynamic factors. Venous congestion was responsible for progressive symptoms. Acute deficits unrelated to bleeds were due to intralesional thrombosis or hemodynamic changes., Interpretation: The short term prognosis of hemorrhagic SCAVSs is good, and there is no need for emergency treatment. MRI delineates the cord and makes the diagnosis of the lesion but angiography remains the gold standard for analysis of the vasculature. The angio-architecture reflects the ageing of the lesion but there is not a precise correlation between angio-architecture and clinical symptoms, except for pseudoaneurysms which relate to the hemorrhagic portion of the lesion.

Vascular endothelial growth factor (VEGF) demonstrates potent and well-characterized effects on endothelial cytoprotection and angiogenesis. In an attempt to preserve spinal microvasculature and prolong the endogenous neovascular response observed transiently following experimental spinal cord injury (SCI), exogenous recombinant human VEGF (rhVEGF165) was injected into the injured rat spinal cord. Adult female Fischer 344 rats were subjected to moderate SCI (12.5 g-cm) using the NYU impactor. At 72 h after injury, animals were randomly assigned to three experimental groups receiving no microinjection or injection of saline or saline containing 2 microg of rhVEGF165. Acutely, VEGF injection resulted in significant microvascular permeability and infiltration of leukocytes into spinal cord parenchyma. 6 weeks postinjection, no significant differences were observed in most measures of microvascular architecture following VEGF treatment, but analysis of histopathology in spinal cord tissue revealed profound exacerbation of lesion volume. These results support the idea that intraparenchymal application of the proangiogenic factor VEGF may exacerbate SCI, likely through its effect on vessel permeability.

Injury to the spinal cord results in disruption of neurons, cell membranes, axons, myelin, and endothelial cells. The aim of this study was to demonstrate the protective effect of magnesium sulfate on the blood-spinal cord barrier after acute spinal cord injury (SCI). This experiment was conducted in two parts. In the first, rats were injected intravenously with Evans blue 2 h after SCI. The laminectomy-only group had no trauma. Contusion injury (50 g-cm) was applied to the trauma and treatment groups. Magnesium sulfate (600 mg/kg) was given to the treatment group immediately after injury. For the second part, clinical evaluations were performed 24 h post surgery. Then, following Evans blue injection, spinal cord samples were obtained from the laminectomy-only, trauma, and treatment groups. For the control group, nontraumatized spinal cord samples were taken after Evans blue injection following clinical examination. Laminectomy did not affect the spinal cord Evans blue content in 2-h and 24-h groups. The trauma increased tissue Evans blue content, and 24-h samples showed more remarkable tissue Evans blue content, suggesting secondary injury. Application of 600 mg/kg of magnesium resulted in lower Evans blue content in the spinal cord than with injury. Remarkable clinical neuroprotection was observed in the treatment groups. Magnesium sulfate showed vaso- and neuroprotective properties after contusion injury to the rat spinal cord. The authors also demonstrated secondary injury of the blood-spinal cord barrier with the Evans blue clearance technique for the first time.

Spinal dural AVFs, the most common type of spinal arteriovenous malformations, are symptomatic because of venous hypertension and congestion. This has been referred to as venous congestive myelopathy. The typical MRI findings that reflect venous congestive myelopathy include peripheral T2 hypointensity that outlines a T2 hyperintensity within a swollen spinal cord. Enlarged perimedullary vessels are typically present. Contrast-enhanced MRA has become instrumental in localizing the site of these fistulas. Spinal epidural AVFs and the perimedullary spinal cord AVFs may also present with a congestive myelopathy and have similar findings on MRI. Angiography remains the gold standard for characterization of the angioarchitecture of spinal vascular malformations. [figure: see text] Multidisciplinary treatment planning is mandatory and requires knowledge of the natural history of these vascular lesions.

Spinal column pathology plays an important role in the etiology and pathogenesis of acute and chronic spinal blood supply disturbances. The aim of the study was to determine a role of degenerative-dystrophic changes, arising as a consequence of Scheuermann's disease in a mechanism of this pathology development. In patients aged 17-65 years, subjected to study of the causes of acute (8 cases) and chronic (7 cases) ischemic spinal disturbances development a significance of spinal column structures changes in juvenile kyphosis for evolution of spinal cord vascular pathology was established.

Objective: To assess the diagnosis and treatment of venous hypertensive myelopathy (VHM) caused by narrowing of the ascending lumbar vein., Method: The data from 3 patients with VHM caused by narrowing of the ascending lumbar vein were analyzed retrospectively., Results: Once the narrowed site of the lumbar ascending vein was determined by myelographic or angiographic technique, an undetachable balloon was introduced and advanced to the proximal part of the narrowed segment. Satisfactory results were obtained in these patients., Conclusion: Narrowing of the ascending lumbar vein is one of the causes for VHM, and endovascular balloon angioplasty is an optimal treatment.

Study Design: A case was reported in which paradoxical air embolism arose from the patent foramen ovale in scoliosis surgery., Objectives: To present a case of suspected paradoxical air embolism after scoliosis surgery., Summary of Background Data: Embolic accident during scoliosis surgery may be caused by air, thrombus, or fat. There is growing attention on patent foramen ovale involved in paradoxical embolism. The devastating consequences are caused by multiple artery occlusions., Methods: Details of a recent documented neurologic complication (paraplegia, weakness of right arm, and blurry vision) after scoliosis surgery have been analyzed in medical publications., Results: The surgical procedure was not imputed. The causative role of epidural catheter for analgesia was considered, but it is likely that a paradoxical embolism occurred in this case, based on the multifocal (cerebral and spinal) neurologic dysfunction, the evidence of cerebral ischemia (on computed tomography), and the presence of a patent foramen ovale (on postoperative transesophageal echocardiography). Although no intraoperative embolism detection was available, air embolism was highly suspected because there was no absolute argument to exclude cruor or fatty embolism., Conclusions: It is critical to detect a patent foramen ovale before surgery and cerebral embolization intraoperatively. This might permit ascertainment of the etiologic diagnosis in case of a complication in surgery for scoliosis.

Background: Spinal cord arteriovenous malformation (AVM) associated with spinal aneurysm is not particularly rare, but cases presenting with hematomyelia are relatively rare compared to those with subarachnoid hemorrhage (SAH). We report a rare case of successfully treated spinal AVM associated with ruptured aneurysm presenting with hematomyelia., Case Description: A 52-year-old male was admitted to our hospital with sudden onset of tetraplegia, respiratory disturbance, and superficial sensory disturbance. Computed tomography revealed hematomyelia at the level of C3-4. Gadolinium-enhanced magnetic resonance imaging showed small, enhanced lesions. Angiography revealed an intradural perimedullary arteriovenous malformation associated with two aneurysms on the feeding arteries. Administration of high-dose methylprednisolone gradually ameliorated his symptoms. Direct surgical obliteration was performed on the 30th day after the onset. The bilateral C3 cervical radicular arteries and the nidus were coagulated. Angiography performed after surgery showed neither the aneurysms nor the nidus. He was discharged with only mild weakness in the left upper extremity and mild left hypesthesia 3 months after surgery, and was fully independent., Conclusion: We report a case of hematomyelia caused by ruptured aneurysm associated with spinal arteriovenous malformation that was successfully treated with surgical obliteration.

Background and Purpose: MR findings reported in conjunction with spinal dural arteriovenous fistula (SDAVF) include cord swelling, increased T2 signal within the spinal cord, and parenchymal enhancement, each of which is nonspecific. Enlarged vessels on the cord surface, the most specific MR finding, is noted in only half of SDAVF patients. Nevertheless, we have frequently observed MR peripheral hypointensity of the spinal cord in SDAVF on T2-weighted images, which is not characteristic of nonvascular or nonhemorrhagic causes of myelopathy and which has not been described in association with SDAVF. We hypothesized that peripheral cord hypointensity might reliably suggest the diagnosis of SDAVF or other causes of venous hypertensive myelopathy., Methods: We reviewed the MR findings in 11 consecutive cases of angiographically confirmed symptomatic SDAVF and in four cases of intracranial dural arteriovenous fistula with spinal drainage, a lesion that also causes spinal cord deficits mediated by venous hypertensive myelopathy., Results: In each case, T2 hypointensity involving the cord periphery was present. This sign has not been previously described in association with either SDAVF or other causes of venous hypertensive myelopathy. It appears, however, to be a relatively constant imaging feature of SDAVF., Conclusion: In the absence of spinal hemorrhage, T2 hypointensity involving the periphery of the spinal cord suggests venous hypertensive myelopathy as a cause of spinal cord dysfunction.

We reported a case of simultaneous medullary hemorrhage and hematomyelia. A 93-year-old woman, who had hypertension, was admitted to our hospital because of headache, numbness and weakness of the left extremities, and somnolence. On admission, weakness and disturbance of tactile sensations were observed in the left extremities. Magnetic resonance imaging showed medullary hemorrhage and hematomyelia and these two lesions were separated. Medullary hemorrhage was at the left dorsal paramedian area within mid-lower medulla oblongata, and hematomyelia was at the left side of the gray matter from medullo-cervical junction to upper cervical cord. Five days later from admission, weakness occurred in the right lower extremity and also in the upper extremity. This process suggested that the main lesion of tetraparesis was medullo-cervical junction. Review of 16 cases of medullary hemorrhage demonstrated that frequent neurological signs were palatal weakness, nystagmus, and disturbance of pain and temperature sense. But our case showed only disturbance of tactile sensations. Review of 19 cases of hematomyelia demonstrated that frequent neurological signs were sensory disturbance, paralysis and localized pain. Our case showed only paralysis. The cause of simultaneous hemorrhage was considered arteriovenous malformation or simultaneous multiple hypertensive hemorrhages.