Cranial and sacral dural arteriovenous fistulas as a cause of myelopathy

1992 ◽  
Vol 76 (4) ◽  
pp. 615-622 ◽  
Author(s):  
Michael D. Partington ◽  
Daniel A. Rüfenacht ◽  
W. Richard Marsh ◽  
David G. Piepgras
Keyword(s):  
Spinal Cord ◽  
Magnetic Resonance Images ◽  
Venous Hypertension ◽  
Spinal Cord Tissue ◽  
Pathophysiological Mechanism ◽  
Content Type ◽  
Av Fistula ◽  
Av Fistulas ◽  
Spinal Dural Av Fistula ◽  
Fine Print

✓ The authors report a series of seven patients with myelopathy who were found to have spinal dural arteriovenous (AV) fistulas in which the nidus was located at some distance from the spinal cord. The nidus was intracranial in three cases and involved a sacral nerve root sheath in the other four, in each case, the arterialized draining vein led into the coronal plexus of medullary veins. A lack of normal draining radicular veins was noted in all cases. Magnetic resonance images were obtained in four patients and demonstrated spinal cord tissue changes only in the lower thoracic cord in three cases and in the cervical cord in one, all consistent with an ischemic process secondary to venous hypertension. Five patients were managed surgically by division of the draining vein, with improvement of the neurological deficit in all. One patient was treated by embolization alone and had stabilization of her deficit. The remaining patient in the series died of unrelated systemic disease before the spinal dural AV fistula could be treated. These cases support the theory that venous hypertension is the dominant pathophysiological mechanism involved in spinal dural AV fistulas independent of their location. In patients with a suspected spinal dural AV fistula, lumbar and thoracic spinal angiography will reveal the site of the fistula in the majority of cases (88% in this series). In the remaining patients, the possibility of a remote fistula must be considered. The lack of normal venous drainage of the cord following injection in the artery of Adamkiewicz is the most reliable indicator of venous hypertension in the cord and can be helpful in making the decision to proceed with a search for a cranial or sacral arterial supply.

Myelopathy due to intracranial dural arteriovenous fistulas draining intrathecally into spinal medullary veins

1988 ◽  
Vol 69 (6) ◽  
pp. 934-939 ◽  
Author(s):  
Charles J. Wrobel ◽  
Edward H. Oldfield ◽  
Giovanni Di Chiro ◽  
Edward C. Tarlov ◽  
Richard A. Baker ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Venous Hypertension ◽  
External Carotid ◽  
Pathophysiological Mechanism ◽  
Partial Recovery ◽  
Content Type ◽  
Av Fistula ◽  
Progressive Myelopathy ◽  
Cord Injury ◽  
Av Fistulas

✓ Arteriovenous malformations (AVM's) of the spine commonly cause progressive myelopathy. Occasionally, myelography reveals serpentine filling defects characteristic of a spinal AVM, but an AVM or arteriovenous (AV) fistula cannot be demonstrated arteriographically, despite selective catheterization of all vessels known to have the potential of supplying the spinal cord and spinal dura. Often, and particularly in the setting of subacute or acute deterioration, this has been attributed to spontaneous thrombosis of the veins (the Foix-Alajouanine syndrome). Three patients are reported in whom intracranial dural AV fistulas, supplied by branches of the internal and external carotid arteries, drained into spinal veins and produced myelopathy. In one patient, motor and sensory deficits were limited to the lower extremities. In all three patients, disconnection of the fistula from its spinal venous drainage permitted arrest of a rapidly progressive myelopathy and partial recovery. These findings indicate that some patients who appear to have spinal cord AVM's but exhibit negative spinal arteriography are suffering from cranial dural AV fistulas and therefore need carotid as well as spinal arteriography. The considerable distance of these fistulas from the level of neurological expression supports venous hypertension as a pathophysiological mechanism of spinal cord injury. Interruption of a cranial dural fistula draining into spinal veins permits recovery of the myelopathy.

A variant of arteriovenous fistulas within the wall of dural sinuses. Results of combined surgical and endovascular therapy

1991 ◽  
Vol 74 (2) ◽  
pp. 199-204 ◽  
Author(s):  
Stanley L. Barnwell ◽  
Van V. Halbach ◽  
Christopher F. Dowd ◽  
Randall T. Higashida ◽  
Grant B. Hieshima ◽  
...  
Keyword(s):  
Venous Drainage ◽  
Venous Hypertension ◽  
Neurological Dysfunction ◽  
Dural Sinus ◽  
Unique Type ◽  
Content Type ◽  
Av Fistula ◽  
Arteriovenous Fistulas ◽  
Av Fistulas ◽  
Cortical Venous Drainage

✓ Dural arteriovenous (AV) fistulas are thought to be acquired lesions that form in an area of thrombosis within a sinus. If the sinus remains completely thrombosed, venous drainage from these lesions occurs through cortical veins, or, if the sinus is open, venous drainage is usually into the involved sinus. Among 105 patients with dural A V fistulas evaluated over the the past 5 years, seven had a unique type of dural AV fistula in the superior sagittal, transverse, or straight sinus in which only cortical venous drainage occurred despite a patent involved sinus; the fistula was located within the wall of a patent dural sinus, but outflow was not into the involved sinus. This variant of dural AV fistulas puts the patient at serious risk for hemorrhage or neurological dysfunction caused by venous hypertension. Three patients presented with hemorrhage, one with progressive neurological dysfunction, one with seizures, and two with bruit and headaches. A combination of surgical and endovascular techniques was used to close the fistula while preserving flow through the sinus.

Effect of anti—rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5′-triphosphatase and superoxide dismutase activation, and ultrastructural changes

2001 ◽  
Vol 95 (1) ◽  
pp. 64-73 ◽  
Author(s):  
Metin Tuna ◽  
Sait Polat ◽  
Tahsin Erman ◽  
Faruk Ildan ◽  
A. Iskender Göçer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Tissue ◽  
Inos Activity ◽  
Content Type ◽  
Cord Injury ◽  
Oxide Synthase ◽  
Fine Print ◽  
Inducible Nitric Oxide

Object. The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti—rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5′-triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment. Methods. Seventy rats were randomly allocated to four groups. Group I (10 rats) were killed to provide normal spinal cord tissue for testing. In Group II 20 rats underwent six-level laminectomy for the effects of total laminectomy alone to be determined. In Group III 20 rats underwent six-level T2–7 laminectomy and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 Group IV rats, but these rats also received one (2 µg) intraperitoneal injection of anti—rat IL-6 antibody immediately after the injury and a second dose 24 hours posttrauma. Half of the rats from each of Groups II through IV were killed at 2 hours and the other half at 48 hours posttrauma. The exposed cord segments were immediately removed and processed for analysis. Conclusions. The results showed that neutralizing IL-6 bioactivity with anti—rat IL-6 antibody significantly attenuates iNOS activity and reduces secondary structural changes in damaged rat spinal cord tissue.

Presence and significance of CD-95 (Fas/APO1) expression after spinal cord injury

2001 ◽  
Vol 94 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Mercedes Zurita ◽  
Jesús Vaquero ◽  
Isabel Zurita
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
Spinal Cord Tissue ◽  
Injured Spinal Cord ◽  
Content Type ◽  
Cord Injury ◽  
Positive Immunostaining ◽  
Fine Print

Object. A glycoprotein, CD95 (Fas/APO1) is widely considered to be implicated in the development of apoptosis in a number of tissues. Based on the hypothesis that apoptosis is related to cell death after spinal cord injury (SCI), the authors studied the presence and distribution of CD95 (Fas/APO1)-positive cells in injured spinal cord tissue for the purpose of determining the significance of this protein during the early phases of SCI. Methods. The presence and distribution of cells showing positive immunostaining for CD95 (Fas/APO1) were studied 1, 4, 8, 24, 48, and 72 hours and 1, 2, and 4 weeks after induction of experimental SCI in rats. Studies were conducted using a monoclonal antibody to the CD95 (Fas/APO1) protein. Positivity for CD95 (Fas/APO1) was observed in apoptotic cells, mainly in the gray matter, 1 hour after trauma, and the number of immunostained cells increased for the first 8 hours, at which time the protein was expressed in both gray and white matter. From 24 to 72 hours postinjury, the number of immunostained cells decreased in the gray matter, but increased in the white matter. From then on, there were fewer CD95 (Fas/APO1)-positive cells, but some cells in the white matter still exhibited positive immunostaining 1 and 2 weeks after injury. At 4 weeks, there remained no CD95 (Fas/APO1)-positive cells in injured spinal cord. Conclusions. These findings indicate that CD95 (Fas/APO1) is expressed after SCI, suggesting a role for this protein in the development of apoptosis after trauma and the possibility of a new therapeutic approach to SCI based on blocking the CD95 (Fas/APO1) system.

Norepinephrine levels in experimental spinal cord trauma

1977 ◽  
Vol 46 (3) ◽  
pp. 342-349 ◽  
Author(s):  
Stephen E. Rawe ◽  
Robert H. Roth ◽  
Margaret Boadle-Biber ◽  
William F. Collins
Keyword(s):  
Spinal Cord ◽  
Tyrosine Hydroxylase ◽  
Concentration Gradient ◽  
Neurological Function ◽  
Spinal Cord Tissue ◽  
Spinal Cord Trauma ◽  
Content Type ◽  
Spinal Cord Segment ◽  
Fine Print

✓ Levels of norepinephrine (NE) in the spinal cord tissue of nontraumatized cats are highest in the cervical and lumbar enlargements. A rather uniform but slightly increasing concentration gradient from cephalad to caudad is observed in the thoracic segments. A 500 gm-cm trauma at the T-5 or C-7 spinal cord segment did not demonstrate any significant increase in NE levels measured sequentially over a 4-hour period after trauma. Dopamine levels could not be detected in the nontraumatized or traumatized cat spinal cords. Four traumatized cats treated with alpha methyl tyrosine, a tyrosine hydroxylase inhibitor, and followed clinically for 5 months showed no improvement in neurological function when compared to untreated traumatized cats. This study does not support the norepinephrine hypothesis of experimental spinal cord trauma.

Pathological basis of spinal cord cavitation in syringomyelia: analysis of 105 autopsy cases

1995 ◽  
Vol 82 (5) ◽  
pp. 802-812 ◽  
Author(s):  
Thomas H. Milhorat ◽  
Anthony L. Capocelli ◽  
Archinto P. Anzil ◽  
Rene M. Kotzen ◽  
Robert H. Milhorat
Keyword(s):  
Spinal Cord ◽  
Subarachnoid Space ◽  
Fourth Ventricle ◽  
Spastic Paraparesis ◽  
Central Canal ◽  
Spinal Cord Tissue ◽  
Content Type ◽  
Age Related ◽  
Spinal Subarachnoid Space ◽  
Fine Print

✓ This report summarizes neuropathological, clinical, and general autopsy findings in 105 individuals with nonneoplastic syringomyelia. On the basis of detailed histological findings, three types of cavities were distinguished: 1) dilations of the central canal that communicated directly with the fourth ventricle (47 cases); 2) noncommunicating (isolated) dilations of the central canal that arose below a syrinx-free segment of spinal cord (23 cases); and 3) extracanalicular syrinxes that originated in the spinal cord parenchyma and did not communicate with the central canal (35 cases). The incidence of communicating syrinxes in this study reflects an autopsy bias of morbid conditions such as severe birth defects. Communicating central canal syrinxes were found in association with hydrocephalus. The cavities were lined wholly or partially by ependyma and their overall length was influenced by age-related stenosis of the central canal. Noncommunicating central canal syrinxes arose at a variable distance below the fourth ventricle and were associated with disorders that presumably affect cerebrospinal fluid dynamics in the spinal subarachnoid space, such as the Chiari I malformation, basilar impression, and arachnoiditis. These cavities were usually defined rostrally and caudally by stenosis of the central canal and were much more likely than communicating syrinxes to dissect paracentrally into the parenchymal tissues. The paracentral dissections of the central canal syrinxes occurred preferentially into the posterolateral quadrant of the spinal cord. Extracanalicular (parenchymal) syrinxes were found typically in the watershed area of the spinal cord and were associated with conditions that injure spinal cord tissue (for example, trauma, infarction, and hemorrhage). A distinguishing feature of this type of cavitation was its frequent association with myelomalacia. Extracanalicular syrinxes and the paracentral dissections of central canal syrinxes were lined by glial or fibroglial tissue, ruptured frequently into the spinal subarachnoid space, and were characterized by the presence of central chromatolysis, neuronophagia, and Wallerian degeneration. Some lesions extended rostrally into the medulla or pons (syringobulbia). Although clinical information was incomplete, simple dilations of the central canal tended to produce nonspecific neurological findings such as spastic paraparesis, whereas deficits associated with extracanalicular syrinxes and the paracentral dissections of central canal syrinxes included segmental signs that were referable to affected nuclei and tracts. It is concluded that syringomyelia has several distinct cavitary patterns with different mechanisms of pathogenesis that probably determine the clinical features of the condition.

Arteriovenous fistulas of the brain and the spinal cord

1993 ◽  
Vol 79 (1) ◽  
pp. 16-27 ◽  
Author(s):  
Francis H. Tomlinson ◽  
Daniel A. Rüfenacht ◽  
Thoralf M. Sundt ◽  
Douglas A. Nichols ◽  
Nicolee C. Fode
Keyword(s):  
Spinal Cord ◽  
Imaging Techniques ◽  
Neurological Dysfunction ◽  
Arterial Aneurysm ◽  
Cerebral Lesions ◽  
Content Type ◽  
Satisfactory Outcome ◽  
Ultrasound Study ◽  
Av Fistulas ◽  
Fine Print

✓ Arteriovenous (AV) fistulas of cerebral and spinal arteries are characterized angiographically by an immediate AV transition without a capillary bed or “nidus” as occurs in AV malformations (AVM's). The clinical presentation, morphology, radiology, and treatment of 12 patients with cerebral AV fistulas and of 12 patients with spinal AV fistulas are reviewed. In the patients with cerebral lesions, headache and seizure disorders were the most common presentations followed by subarachnoid hemorrhage, cardiac failure, progressive neurological dysfunction, and incidental detection on prenatal ultrasound study. In patients with spinal AV fistulas, weakness and sensory disturbance in the lower extremities were the most frequent clinical presentations followed by back pain, disturbances of micturition, and grand mal seizure. The etiology of the symptom complex produced by AV fistulas in each of these locations differed, with venous hypertension being important in spinal cord lesions. Of the patients with cerebral lesions, nine had a single AV fistula, one had two fistulas, and two had multiple fistulas. An AVM was observed in five patients with fistulas (two large, three small). Nine patients exhibited extramedullary AV fistulas of the spine, of whom eight had a single fistula and one had three fistulas; three patients had intramedullary spinal AV fistulas. An arterial aneurysm was found in association with two fistulas, one cerebral and one spinal. Venous ectasias or varices, frequently exhibiting mural calcification, were observed to be prominent in all AV fistulas involving cerebral arteries and in two involving spinal arteries. The location and size of the venous complexes reflected the diameter of the fistula. In addition to conventional imaging techniques (cerebral angiography, computerized tomography, and magnetic resonance (MR) imaging), MR angiography was a helpful adjunct in the evaluation of fistulas. Treatment strategies employed for AV fistulas in both locations included open surgical and endovascular procedures, frequently used in combination. A satisfactory outcome was observed in all patients.

The presence of 4-hydroxynonenal/protein complex as an indicator of oxidative stress after experimental spinal cord contusion in a rat model

1998 ◽  
Vol 88 (5) ◽  
pp. 874-883 ◽  
Author(s):  
Stanley A. Baldwin ◽  
Richard Broderick ◽  
David Osbourne ◽  
Georg Waeg ◽  
Deborah A. Blades ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Protein Complex ◽  
Synaptic Function ◽  
Motor Deficits ◽  
Spinal Cord Tissue ◽  
Injury Site ◽  
Content Type ◽  
Spinal Cord Contusion ◽  
Fine Print

Object. The authors tested the hypothesis that breach of the blood—spinal cord barrier (BSCB) will produce evidence of oxidative stress and that a similar staining pattern will be seen between 4-hydroxynonenal (HNE)/protein complexes and extravasated immunoglobulin G (IgG). Methods. Adult female Fischer 344 rats, each weighing 200 to 225 g, were subjected to a spinal cord contusion at T-10 by means of a weight-drop device. Spinal cord tissue was assessed for oxidative stress by localizing extravasated plasma contents with a monoclonal antibody for rat IgG and protein conjugation with HNE, which is an aldehyde byproduct of lipid peroxidation. The animals were killed at 1 and 6 hours, and 1, 2, and 7 days after surgery. Maximum HNE/protein staining was observed at 2 days postinjury, and HNE/protein and IgG manifested similar staining patterns. Analysis revealed a graduated but asymmetrical rostral—caudal response relative to the T-10 injury site. Both HNE/protein complex and IgG staining revealed that the caudal levels T-11 and T-12 stained significantly more intensely than the rostral levels T-9 and T-8, respectively. A higher percentage of neurons positive for HNE/protein immunostaining was observed in spinal cord levels caudal to the injury site compared with equidistant rostral regions. Protein dot-blot assays also revealed a similar asymmetrical rostral—caudal HNE/protein content. To analyze the timing of the BSCB breach, another group of animals received identical contusions, and horseradish peroxidase (HRP) was injected 10 minutes before or at various times after injury (1, 3, and 6 hours, and 1, 2, and 7 days). Maximum HRP permeability was seen immediately after injury, with a significant decrease occurring by 1 hour and a return to control levels by 2 days posttrauma. Conclusions. Data from this study indicate possible compromise of neuronal, axonal, glial, and synaptic function after trauma, which may be a factor in motor deficits seen in animals after spinal cord contusion. The colocalization of the IgG stain with the HNE/protein stain is consistent with the hypothesis of a mutual cause—effect relationship between BSCB and oxidative stress in central nervous system trauma.

Ischemia in primate spinal cord injury

1971 ◽  
Vol 34 (5) ◽  
pp. 614-617 ◽  
Author(s):  
George E. Locke ◽  
David Yashon ◽  
Robert A. Feldman ◽  
William E. Hunt
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Lactic Acid ◽  
Rhesus Monkeys ◽  
Spinal Cord Tissue ◽  
Time Intervals ◽  
Content Type ◽  
Lactate Accumulation ◽  
Cord Injury ◽  
Fine Print

✓ Lactate accumulation in spinal cord tissue following trauma was determined to ascertain the role and magnitude of ischemia. High thoracic and low thoracic laminectomies were performed on each of nine rhesus monkeys. The lower exposed cord was traumatized with a calibrated blow of 300 gm cm. The upper exposed cord served as a nontraumatized control. At time intervals of 1.5 min to 48 hrs after trauma, both cord segments were removed and assayed for lactic acid. Lactate in nontraumatized segments averaged 3.64 mM/kg tissue, with a range of 2.20 to 4.95. Lactate in traumatized segments removed in from 1.5 min to 12 hrs from six monkeys averaged 5.50 mM/kg tissue, with a range of 4.32 to 6.46. Lactate in traumatized segments from three monkeys 18 to 40 hrs after trauma averaged 4.07 mM/kg, with a range of 3.20 to 5.18. This finding supports the concept that ischemia plays a role early in the traumatic process in spinal cord injury.

Successful treatment of a group of spinal cord arteriovenous malformations by interruption of dural fistula

1983 ◽  
Vol 59 (6) ◽  
pp. 1019-1030 ◽  
Author(s):  
Edward H. Oldfield ◽  
Giovanni Di Chiro ◽  
Eugene A. Quindlen ◽  
Kenneth G. Rieth ◽  
John L. Doppman
Keyword(s):  
Spinal Cord ◽  
Arteriovenous Fistula ◽  
Arteriovenous Malformations ◽  
Venous Hypertension ◽  
Current Therapy ◽  
Type I ◽  
Content Type ◽  
Symptoms And Signs ◽  
Extensive Surgery ◽  
Fine Print

✓ As demonstrated by selective spinal cord arteriography, over 80% of spinal cord arteriovenous malformations (AVM's) occupy a predominantly extramedullary position. Current therapy frequently requires surgical stripping of the long dorsal intradural vessel(s) from the underlying spinal cord over many cord segments. The authors report six patients with a dural arteriovenous fistula fed by a cluster of abnormal epidural arteries. These vessels, which surrounded and were embedded into the dural covering of a thoracic nerve root, drained into a long sinuous intrathecal paramedullary vein(s). The angiographic and surgical appearance of the intradural component of these lesions was identical to that of lesions previously classified as Type I AVM's of the spinal cord. All patients had symptoms and signs of myelopathy. In five patients, surgery was limited to coagulation and excision of the extradural vessels and division of the intradural arterialized vein. Progressive improvement began within days following surgery. No residual abnormality was demonstrated by postoperative selective spinal cord arteriography, which was performed in all five patients. The findings support those of Kendall and Logue, that surgery restricted to elimination of the arteriovenous fistula at the intervertebral foramen is curative, and that more extensive surgery is unnecessary for this subgroup of AVM's of the spinal cord. These lesions comprise a sizable percent of all spinal AVM's. Resolution of myelopathy in these patients supports the hypothesis that venous hypertension causes chronic progressive myelopathy.

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