Reversible acute and subacute myelopathy in patients with dural arteriovenous fistulas

Foix-Alajouanine syndrome reconsidered

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✓ Acute or subacute neurological deterioration without evidence of hemorrhage in a patient with a spinal arteriovenous (AV) malformation has been referred to as “Foix-Alajouanine syndrome.” This clinical entity has been considered to be the result of progressive vascular thrombosis resulting in a necrotic myelopathy; it has therefore been thought to be largely irreversible and hence untreatable. The authors report five patients with dural AV fistulas who presented in this manner, and who improved substantially after embolic and surgical therapy. The outcome of these patients indicates that acute and subacute progression of myelopathy in cases of spinal dural AV fistulas may be caused by venous congestion and not necessarily by thrombosis. Therefore, a clinical diagnosis of Foix-Alajouanine syndrome is of little practical use, as spinal cord dysfunction from venous congestion is a potentially reversible process whereas thrombotic infarction is not. This diagnosis may result in suboptimal management. The recognition of nonhemorrhagic acute or subacute myelopathy as a complication of a spinal dural AV fistula is important since what appears to be irreversible cord injury is often treatable by standard surgical techniques.

Abstract

✓ Acute or subacute neurological deterioration without evidence of hemorrhage in a patient with a spinal arteriovenous (AV) malformation has been referred to as “Foix-Alajouanine syndrome.” This clinical entity has been considered to be the result of progressive vascular thrombosis resulting in a necrotic myelopathy; it has therefore been thought to be largely irreversible and hence untreatable. The authors report five patients with dural AV fistulas who presented in this manner, and who improved substantially after embolic and surgical therapy. The outcome of these patients indicates that acute and subacute progression of myelopathy in cases of spinal dural AV fistulas may be caused by venous congestion and not necessarily by thrombosis. Therefore, a clinical diagnosis of Foix-Alajouanine syndrome is of little practical use, as spinal cord dysfunction from venous congestion is a potentially reversible process whereas thrombotic infarction is not. This diagnosis may result in suboptimal management. The recognition of nonhemorrhagic acute or subacute myelopathy as a complication of a spinal dural AV fistula is important since what appears to be irreversible cord injury is often treatable by standard surgical techniques.

In 1926, Foix and Alajouanine5 described two patients with subacute myelopathy produced by a thrombotic disorder of the spinal cord that ultimately caused death. Postmortem examination of the spinal cord revealed extensive vascular thrombosis, spinal cord necrosis, and many abnormally dilated, tortuous, thick-walled surface vessels. Lhermitte, et al.,10 in 1931 recognized the association of this process with an arteriovenous malformation (AVM) of the spinal cord. Later, Wyburn-Mason,17 Flament, et al.,4 and Wirth, et al.,16 reaffirmed the association between rapidly progressive myelopathy, vascular thrombosis, and abnormal spinal cord vasculature. Pia and Vogelsang13 concluded that Foix-Alajouanine disease was not a distinct entity but a complication of spinal AVM's that was caused by thrombosis within the abnormal vessels of the spinal cord. Wirth, et al., concurred with this view of the pathophysiology of this syndrome, and first described a patient in whom chronic clinical deterioration was correlated with the finding at surgery of an extensively thrombosed AVM and spinal cord atrophy. They reemphasized the futility in treating patients with this condition, as they considered it an end-stage process without hope of useful recovery of function.

Five patients with spinal dural arteriovenous (AV) fistulas who experienced acute or subacute onset of myelopathy in the absence of hemorrhage are described here. Therapeutic intervention, including anticoagulation, embolization, and surgical ablation of the dural AV fistula, stabilized or reversed neurological deterioration in these patients. Partial but significant recovery occurred in most patients. Our experience indicates that in the early stages of acute or subacute myelopathy caused by spinal dural AV fistulas the pathophysiology is venous congestion, not thrombosis. Therefore, in patients with spinal dural AV fistulas and rapidly progressive myelopathy (Foix-Alajouanine syndrome), the myelopathy is probably caused by deterioration of the compensatory capacity of the spinal cord to accommodate venous congestion (compensation/decompensation phenomenon). This departure from classical observations is important clinically in that early diagnosis and proper management of venous congestion are likely to result in a successful outcome.

Case Reports
Case 1

This 61-year-old retired male property manager developed progressive weakness and sensory loss in this lower extremities, urinary incontinence, and constipation, all occurring over 4 weeks. On the day of admission to the Clinical Center at the National Institutes of Health (NIH), complete paralysis of his lower extremities and a progressive ascending sensory deficit developed over several hours.

First Admission

Neurological examination revealed flaccid paraplegia, complete sensory loss below T-10, and diminished rectal sphincter tone. There was no spinal bruit or cutaneous hemangioma. The patient was given intravenous dexamethasone and was anticoagulated with heparin, without evidence of clinical improvement. At spinal arteriography, selective injection of the right lumbar artery at L-2 showed a dural AV fistula at L-2 with a characteristic vein draining the blood from the fistula into the subarachnoid veins. The dural AV fistula was occluded by embolization with 250- to 500-mµ particles of polyvinyl alcohol (Ivalon). Within 24 hours of the embolization, motor and sensory function began to recover. Follow-up arteriography 5 days after the first study revealed persistent flow through the AV fistula and persistent opacification of the spinal vein. A previously unrecognized L-3 feeder vessel was demonstrated and was embolized with 250- to 500-mµ particles until flow through the AV fistula was eliminated. The patient was discharged after regaining antigravity strength and with improving sensory function, but without voluntary control of bowel or bladder function.

Second Admission

As his recovery progressed, the patient was able to walk using parallel bars but could not ambulate independently. He regained normal lower-extremity sensation but still required self-catheterization. On the day before admission, he rapidly became paraplegic and was given intravenous dexamethasone. He regained antigravity function that evening. Early the next morning he again lost all lower-extremity function and had been in that condition for approximately 12 hours at admission. He had flaccid paraplegia with total loss of sensation below T-10. There was no response to plantar stimulation, and deep tendon, abdominal, and cremasteric reflexes were absent. Repeat selective spinal arteriography 60 days after the first embolization revealed reestablishment of flow through the spinal dural AV fistula at L-2. Both the L-2 and L-3 feeder vessels were occluded by embolization with 125- to 250-mµ polyvinyl alcohol particles. Motor and sensory function began to recover within hours after embolization. Within 48 hours, the patient regained some antigravity function and no longer had a detectable sensory level. Four days after embolization, heparin therapy was discontinued and the patient underwent surgery.

Operation

Laminectomy of L1–3 with an L2–3 foraminotomy on the right exposed the cluster of tortuous arteries surrounding and embedded in the L-2 nerve root sleeve and the adjacent spinal dura. The AV fistula was drained by a single intrathecal vessel which traversed the subarachnoid space to join the coronal venous plexus on the ventral surface of the spinal cord. There were several small areas of thrombosis in radicular veins at isolated nerve roots. The feeding vessels and nidus of the AV fistula were coagulated as they entered the dura, and the vessel draining the fistula was interrupted as it pierced the inner layer of the dura. Five to 10 minutes after the fistula was interrupted, small areas of plasma-blood layering developed and new thrombosis could be seen through the thin wall of the tortuous thin-walled veins on the cord surface.

Postoperative Course

Lower-extremity strength gradually improved following surgery. Two weeks later, the patient had regained bilateral proximal antigravity strength and had only minimally impaired position sense in the left leg with normal position sense in the right leg. He was discharged on intermittent urinary catheterization. At 14 months after surgery, slow but progressive improvement continued. He was able to walk unaided approximately 150 yards. The previous impairment of position sense had fully resolved and he was voiding voluntarily without urinary retention.

Case 2

This 56-year-old male machinist has been described previously.12 He developed urinary hesitancy and weakness in his left leg 5 months before admission. His condition remained stable for several months and he was able to walk limited distances. His neurological deficit worsened dramatically over the 2 weeks before admission and he became confined to a wheelchair.

Admission

On admission he could walk a distance of only several feet with the aid of a cane. He developed perineal numbness and urinary retention requiring placement of an indwelling urinary catheter. Myelography showed a long serpentine filling defect throughout the thoracolumbar subarachnoid space.

Neurological examination revealed lower-extremity weakness bilaterally (greater on the left than the right). Pinprick and cold sensation was impaired below L-4. Joint position sense was intact and Romberg's sign was negative. Deep-tendon reflexes were hyperactive at the knees and the left ankle, and the plantar response was extensor on the left. There was spasticity to passive flexion and sustained clonus of the left ankle. The patient had a wide-based unsteady gait. There was no spinal bruit or cutaneous hemangioma. Selective spinal arteriography showed a cluster of abnormal vessels at the T9–10 intervertebral foramen, indicating a dural AV fistula that was fed from the right ninth intercostal artery.

Operation

Laminectomy of T-9 and T-10 and foraminotomy at T9–10 exposed a cluster of epidural arteries surrounding the T-9 nerve root. The vessels draining the dural fistula entered the dura as a single arterialized vein which drained the fistula into the tortuous dilated coronal venous plexus on the dorsal surface. No thrombosed veins were evident. After interruption of the arterial supply and the intradural venous drainage, the dural fistula was coagulated.

Postoperative Course

Following surgery, the patient's neurological deficits improved daily. Within 2 weeks his strength returned to normal, and the numbness of the left leg and perineum resolved. He walked without difficulty and his urinary bladder function returned. Postoperative spinal arteriography did not opacify the previously demonstrated abnormality. When seen 3 months later, he had normal motor and sensory function, although paresthesias of the perineum persisted.

Case 3

This 68-year-old male lobbyist had a long history of lower-extremity claudication. Peripheral vascular evaluation was negative except for hypertension. He developed paraparesis following surgery for a malignant bladder tumor in July, 1986. At that time he was able to ambulate only with a walker. Six months later, he was able to walk 0.4 mile with the aid of a cane; greater distances were limited by a diffuse heavy feeling in both legs without sensory difficulties. In January, 1987, he developed progressive lower-extremity weakness (greater on the right than the left), gait deterioration, right-sided foot drop, spontaneous myoclonus, and ascending sensory loss to the waist. Myelography and magnetic resonance imaging showed tortuous dilated surface vessels from the lumbar to upper cervical levels. Spinal arteriography failed to demonstrate the cause of myelopathy, and the patient was transferred to the NIH.

Admission

Examination revealed spastic paraparesis with absent antigravity function and an extensor plantar response on the left. Sensory examination showed a bilateral L1–2 level to pinprick and light touch sensation with preservation of joint position sense. There was no sacral sparing of pinprick sensibility. No spinal bruit or cutaneous hemangioma could be identified. Spinal arteriography failed to disclose the spinal AV fistula, but a complete study could not be performed because several lower thoracic and upper lumbar intercostal arteries had been occluded by severe aortic atherosclerosis.

Operations

Because of the rapidity of progression and the severity of myelopathy, and since spinal AVM's which become symptomatic in late adulthood are most often dural AV fistulas at the lower thoracic and upper lumbar levels, a laminectomy and exploratory intradural dissection were performed from T-10 to L-4. Enlarged tortuous posterior spinal veins free of thrombus were encountered throughout the length of the exposed cord, but the site of the nidus of a spinal dural AV fistula could not be identified.

Postoperatively, the patient had significant progression of his deficit, leaving him with no voluntary movement of the lower extremities. Joint position sense was intact at the ankles but absent in the toes. Left external and internal carotid arteriography opacified a dural AV fistula of the tentorium. The fistula drained into the subarachnoid space and inferiorly to fill the abnormal, tortuous, dilated spinal veins. Six days after the laminectomy, the patient underwent a suboccipital craniectomy and interruption of the dural (tentorial) arteriovenous fistula.

Postoperative Course

The patient's immediate postoperative neurological examination was unchanged from his preoperative status. He had a flaccid paraplegia with occasional flexor spasms and a sensory level at T12-L1 without sacral sparing. Rectal tone was decreased and joint position sense was lost in both legs. Plantar responses were extensor bilaterally. On the following day joint position sense was present. He regained movement against gravity at the ankles and toes but had no functionally significant improvement. He was discharged to a rehabilitation hospital with an indwelling urinary drainage catheter. Four months later urinary catheterization was no longer necessary, although he had no further motor improvement.

Case 4

This 60-year-old male dock worker has been described previously.12 He developed weakness of his legs 1 year before admission and within 5 months stopped working due to progressive weakness and frequent falls. Two months before admission he developed bowel and bladder incontinence, and was admitted to a local hospital. Myelography demonstrated tortuous abnormal filling defects from the midthoracic to the midlumbar level.

Admission

Neurological examination disclosed a mild symmetrical weakness of his lower extremities, with spasticity at the knees and clonus of the left ankle. Vibratory sensation was absent in the legs and feet, as was pinprick and cold sensation below the L-1 dermatome. His gait was wide-based. Except for his weight of 285 lbs, the patient's general physical examination was normal. There was no cutaneous hemangioma or spinal bruit. Efforts to demonstrate the AVM by selective spinal arteriography were unsuccessful on two occasions due to severe aortic atherosclerosis involving several lumbar and lower thoracic intercostal arteries.

Operations

The patient's recent neurological deterioration prompted exploratory surgery in an attempt to find and interrupt the arterial supply to a spinal dural AV fistula. After a laminectomy at T9–12, the dura was opened to expose tortuous thin-walled red vessels covering both the ventral and dorsal surfaces of the spinal cord. The laminectomy was extended in stages to include T5-L3. The area of dural penetration of each nerve root from T-5 to L-2 was carefully examined, but no vessel was found entering the subarachnoid space from the dura and no intramedullary AVM of the spinal cord was identified. A normal-caliber artery of Adamkiewicz was identified, which entered the dura with the left T-9 nerve root.

Three days postoperatively, the patient's legs became weaker and he developed urinary retention and bowel incontinence. At repeat selective spinal arteriography, contrast injection into the left L-3 artery revealed a dural AV fistula in the L3–4 intervertebral foramen, which emptied into the venous system of the spinal cord. Flow of contrast material through this vessel filled the dilated coiled vessels of the coronal venous plexus from T-5 to L-5. At reoperation, a laminectomy of L-4 and foraminotomy of L3–4 exposed the dural AV fistula, which was interrupted and coagulated.

Postoperative Course

Within 2 to 3 days after surgery, the patient began regaining power in the lower extremities, and sensation to pinprick, cold, position, and vibration improved. When evaluated 6 weeks postoperatively, he was walking with the aid of a cane, and no longer suffered bladder or bowel incontinence. At follow-up evaluation 3½ years after surgery, he still requires a cane for ambulation, but has recovered normal sensory, bowel, and bladder function.

Case 5

This 59-year-old man was working as a supervisory engineer in a steel mill in 1982 when he first developed gradually progressive paraparesis and ascending lower-extremity numbness. In the spring of 1984, he was diagnosed as having lumbar stenosis and underwent a two-level decompressive laminectomy at L-3 and L-4. No improvement was noted. Since myelography had suggested abnormal spinal veins, spinal arteriography was performed but was reported as negative. In the fall of 1984, he required a cane for ambulation and developed overflow incontinence with a neurogenic flaccid bladder. A second spinal arteriogram revealed a dural AV fistula at the T-10 level. Embolization with polyvinyl alcohol resulted in partial recovery of motor strength and sensation over the subsequent 2 or 3 months. However, he once again developed slowly progressive weakness and sensory loss in early 1986, and was evaluated at the NIH Clinical Center in the fall of that year.

Admission

Neurological examination revealed paraparesis with minimal antigravity strength proximally. Lower-extremity deep-tendon reflexes were decreased, tone was normal, and there were no elicitable clonus. Lower abdominal and cremasteric reflexes were absent bilaterally and the plantar responses were flexor. There was a sensory level to pinprick up to T-12 but joint position sense was preserved. Selective spinal angiography revealed the recanalized dural AV fistula at T-10 on the right side.

Operation

Laminectomy of T10–12 and a foraminotomy were performed at T11–12 on the right side. After the dura and arachnoid were opened, a vessel carrying bright red blood was identified as it entered the dura adjacent to the dural penetration on the right T-11 root. The vessel was divided intradurally, and the dural AV fistula was coagulated and excised.

Postoperative Course

The patient had gradual recovery of strength, with improvement over his preadmission status. Follow-up spinal arteriography showed no evidence of persistent filling of the AV fistula. Eleven months later he had continued clinical improvement with only mild weakness, although his original incomplete T-11 sensory level and need for intermittent bladder catheterization remained unchanged.

Discussion

Subacute progressive myelopathy due to partial or complete thrombosis of a spinal AVM is a concept that was introduced by Foix and Alajouanine,5 and was later substantiated by Lhermitte, et al.,10 and others.4,13,16,17 Although the differential diagnosis of subacute myelopathy includes such diverse etiologies as infection, tumor, syringomyelia, toxins, motor neuron disease, and demyelinating disease,1,2,7,8,11 the diagnosis of Foix-Alajouanine syndrome has only been considered when acute and subacute clinical changes occur in a patient with a spinal vascular malformation. The typical clinical findings of progressive paraplegia, sensory changes, and loss of sphincter control are uniformly present but nonspecific. Lumbar puncture revealing elevated CSF protein in the absence of hemorrhage or pleocytosis further suggests this diagnosis. However, albumino-cytological dissociation is also characteristic of postinfectious ascending polyradiculoneuropathy. The rapidity of clinical progression and absence of hemorrhage in a patient with a spinal AVM are the distinctive features that have been collectively designated as the Foix-Alajouanine syndrome.

Rosenblum, et al.,14 recently reviewed 81 cases of spinal AVM's treated at the NIH Clinical Center. The clinical, pathophysiological, and radiographic features were compared in patients with intradural and dural vascular malformations. Dural AV fistulas were demonstrated to present at a later age than intradural AVM's and to typically cause gradually progressive paraparesis, sensory loss, and bladder disturbance (85% of all cases). The vast majority of dural AV fistulas are low-thoracic or lumbar in location, and drainage occurs rostrally in most patients via the coronal venous plexus. Of particular relevance to this report is the observation that 50% of intradural AVM's present acutely, whereas only 10% to 15% of dural AV fistulas present acutely (> 24 hours after identification of spinal AVM's) or subacutely (24 hours to 4 weeks after onset). In intradural AVM's, hemorrhage commonly accompanies acute clinical deterioration, whereas hemorrhage is not associated with acute loss of neurological function in patients with dural AV fistulas.

A variety of pathophysiological mechanisms have been suggested to explain progressive, acute, and subacute myelopathy associated with AVM's of the spinal cord.1–3,6,7,9,11,12,15–17 The high flow of intradural malformations and the common vessel of origin of blood supply to the spinal cord and the AVM are thought to predispose the spinal cord to chronic ischemia resulting from arterial steal. Acute neurological deterioration may be due to spontaneous hemorrhage from aneurysms or vessels of the AVM. Venous congestion, arachnoiditis, and cord compression by aneurysmal blood vessels have also been considered potential mechanisms of cord injury in these patients.

In contrast to the intramedullary AVM's of the spinal cord, dural AV fistulas are low-flow extramedullary lesions. Dural AV fistulas drain intradurally into the coronal venous plexus, which becomes tortuous and elongated with time. The anatomical absence of valves between this plexus and the intramedullary radial veins facilitates the transmission of high venous pressure to cord tissue.12 A venous congestive myelopathy can produce gradually progressive clinical deterioration in these patients. In many instances, however, the initial presentation is accelerated and is therefore reminiscent of apoplectic events such as hemorrhage or thrombosis. This more rapid neurological deterioration on a background of persistent but slowly progressing myelopathy is likely to be related to failure of compensatory mechanisms that allow the spinal cord to function despite the presence of disruption of its normal blood flow regulation. In the setting of cerebral edema, ischemia, and hydrocephalus, this has been referred to as the compensation/decompensation phenomenon.

In patients with spinal dural AV fistulas, venous hypertension and congestion predispose the veins of the spinal cord parenchyma, the radial veins, and the coronal venous plexus to stasis and thrombosis. This is in keeping with the occasional finding of thrombosis in the coronal venous plexus or the radicular veins in these patients, which is associated with a less complete recovery of spinal cord function (Case 1). The rapid progression of venous congestion or the onset of thrombosis of the veins of the spinal cord may explain the observations of Foix and Alajouanine in an era when accurate diagnosis and treatment of spinal AVM's was not possible. However, our observations suggest that in most patients acute or subacute loss of cord function results from increased venous congestion in a cord that has continued to function despite marginally compensated venous hypertension until the onset of the rapidly progressive phase of the myelopathy. In these patients, if the fistula is interrupted and venous hypertension is relieved before irreversible injury by ischemia or venous thrombosis and cord infarction occurs, reversal of myelopathy is possible.

The outcomes of Cases 3 and 4 indicate the importance of preoperative identification, if possible, of the type and site of the spinal AVM. In an attempt to find and interrupt the AV fistula before irreversible injury of the cord occurred, both of these patients received surgery in a setting of rapid, continuing progression of significant neurological deficits. However, both patients lost neurological function as a result of the unsuccessful surgery. This may have been caused by transmission of increased intra-abdominal and intrathoracic pressure to the spinal venous system during surgery in the prone position. An increase in venous pressure during surgery would increase the severity of the preexisting venous hypertension and congestion of the spinal cord, which is the primary mechanism of cord damage in patients with spinal dural AV fistulas. In patients with rapid and significant loss of neurological function, and in whom the site of the dural AV fistula can be identified at arteriography, embolic occlusion of the fistula reduces flow through the fistula and should reduce the venous congestion of the spinal cord so that surgery can be performed with less risk of increasing cord injury intraoperatively. This was performed before surgery in Case 1.

Much knowledge about the classification of spinal AVM's and the mechanism of cord injury with spinal AVM's has been acquired since the development of myelography, spinal arteriography, computerized tomography, and magnetic resonance imaging. However, the potential for a reversal of this process with embolization and surgical ablation of the fistula has only recently become apparent. Our observations indicate that obliteration of the dural AV fistula eliminates the cause of venous congestion and stasis, and can restore spinal cord vascular hemostasis prior to irreversible spinal cord damage. They also argue against Foix-Alajouanine syndrome as a manifestation of venous thrombosis and therefore against the irreversible nature of the cord injury.

References

  • 1.

    Aminoff MJLogue V: Clinical features of spinal vascular malformations. Brain 97:1972101974Brain 97:

  • 2.

    Baker AB: Clinical Neurology. New York: Hoeber-Harper1962Baker AB: Clinical Neurology.

  • 3.

    Di Chiro GDoppman JOmmaya AK: Selective arteriography of arteriovenous aneurysms of spinal cord. Radiology 88:106510771967Radiology 88:

  • 4.

    Flament JVicente ANCoers Cet al: [Angiodysgenetic myelomalacia (Foix-Alajouanine) and its differentiation from spinal necrosis on intramedullary angiomatosis.] Rev Neurol 103:12291960 (Fre)Rev Neurol 103:

  • 5.

    Foix CAlajouanine T: La myélite nécrotique subaique.” Rev Neurol 2:1421926Rev Neurol 2:

  • 6.

    Greenfield JGTurner JWA: Acute and subacute necrotic myelitis. Brain 62:2272521939Brain 62:

  • 7.

    Hoffman HL: Acute necrotic myelopathy. Brain 78:3773931955Hoffman HL: Acute necrotic myelopathy. Brain 78:

  • 8.

    Kahle WSchaltenbrand G: Zur Klinik und Pathologie der Myelitis necroticans diffusa. Dtsch Z Nervenheilk 173:2342661955Dtsch Z Nervenheilk 173:

  • 9.

    Kendall BELogue V: Spinal epidural angiomatous malformations draining into intrathecal veins. Neuroradiology 13:1811891977Neuroradiology 13:

  • 10.

    Lhermitte JFribourg-Blanc AKyriaco N: La gliose angéio-hypertrophique de la moelle épinière (myélite nécrotique de Foix-Alajouanine. Rev Neurol 2:37531931Rev Neurol 2:

  • 11.

    Logue V: Angiomas of the spinal cord: review of the pathogenesis, clinical features, and results of surgery. J Neurol Neurosurg Psychiatry 42:1111979J Neurol Neurosurg Psychiatry 42:

  • 12.

    Oldfield EHDi Chiro GQuindlen EAet al: Successful treatment of a group of spinal cord arteriovenous malformations by interruption of dural fistula. J Neurosurg 59:101910301983J Neurosurg 59:

  • 13.

    Pia HWVogelsang H: Diagnose und Therapie spinaler Angiome. Dtsch Z Nervenheilk 187:74961965Dtsch Z Nervenheilk 187:

  • 14.

    Rosenblum BOldfield EHDoppman JLet al: Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVM“s in 81 patients. J Neurosurg 67:7958021987J Neurosurg 67:

  • 15.

    Symon LKuyama HKendall B: Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases. J Neurosurg 60:2382471984J Neurosurg 60:

  • 16.

    Wirth FP JrPost KDDi Chiro Get al: Foix-Alajouanine disease. Spontaneous thrombosis of a spinal cord arteriovenous malformation: a case report. Neurology 20:111411181970Neurology 20:

  • 17.

    Wyburn-Mason R: The Vascular Abnormalities and Tumours of the Spinal Cord and its Membranes. London: Henry Kimpton1943Wyburn-Mason R: The Vascular Abnormalities and Tumours of the Spinal Cord and its Membranes.

Article Information

Address reprint requests to: Edward H. Oldfield, M.D., Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, 9000 Rockville Pike, Building 10, Room 5D-37, Bethesda, Maryland 20892.

© AANS, except where prohibited by US copyright law.

Headings

References

1.

Aminoff MJLogue V: Clinical features of spinal vascular malformations. Brain 97:1972101974Brain 97:

2.

Baker AB: Clinical Neurology. New York: Hoeber-Harper1962Baker AB: Clinical Neurology.

3.

Di Chiro GDoppman JOmmaya AK: Selective arteriography of arteriovenous aneurysms of spinal cord. Radiology 88:106510771967Radiology 88:

4.

Flament JVicente ANCoers Cet al: [Angiodysgenetic myelomalacia (Foix-Alajouanine) and its differentiation from spinal necrosis on intramedullary angiomatosis.] Rev Neurol 103:12291960 (Fre)Rev Neurol 103:

5.

Foix CAlajouanine T: La myélite nécrotique subaique.” Rev Neurol 2:1421926Rev Neurol 2:

6.

Greenfield JGTurner JWA: Acute and subacute necrotic myelitis. Brain 62:2272521939Brain 62:

7.

Hoffman HL: Acute necrotic myelopathy. Brain 78:3773931955Hoffman HL: Acute necrotic myelopathy. Brain 78:

8.

Kahle WSchaltenbrand G: Zur Klinik und Pathologie der Myelitis necroticans diffusa. Dtsch Z Nervenheilk 173:2342661955Dtsch Z Nervenheilk 173:

9.

Kendall BELogue V: Spinal epidural angiomatous malformations draining into intrathecal veins. Neuroradiology 13:1811891977Neuroradiology 13:

10.

Lhermitte JFribourg-Blanc AKyriaco N: La gliose angéio-hypertrophique de la moelle épinière (myélite nécrotique de Foix-Alajouanine. Rev Neurol 2:37531931Rev Neurol 2:

11.

Logue V: Angiomas of the spinal cord: review of the pathogenesis, clinical features, and results of surgery. J Neurol Neurosurg Psychiatry 42:1111979J Neurol Neurosurg Psychiatry 42:

12.

Oldfield EHDi Chiro GQuindlen EAet al: Successful treatment of a group of spinal cord arteriovenous malformations by interruption of dural fistula. J Neurosurg 59:101910301983J Neurosurg 59:

13.

Pia HWVogelsang H: Diagnose und Therapie spinaler Angiome. Dtsch Z Nervenheilk 187:74961965Dtsch Z Nervenheilk 187:

14.

Rosenblum BOldfield EHDoppman JLet al: Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVM“s in 81 patients. J Neurosurg 67:7958021987J Neurosurg 67:

15.

Symon LKuyama HKendall B: Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases. J Neurosurg 60:2382471984J Neurosurg 60:

16.

Wirth FP JrPost KDDi Chiro Get al: Foix-Alajouanine disease. Spontaneous thrombosis of a spinal cord arteriovenous malformation: a case report. Neurology 20:111411181970Neurology 20:

17.

Wyburn-Mason R: The Vascular Abnormalities and Tumours of the Spinal Cord and its Membranes. London: Henry Kimpton1943Wyburn-Mason R: The Vascular Abnormalities and Tumours of the Spinal Cord and its Membranes.

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