Spinal vascular malformations (angiomas) and myelomalacia

Antoni, Nils

doi:10.1212/wnl.12.11.795

Cited by 41 publications

(8 citation statements)

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“…The case of G reenfield and T urner [7] showed hyaline thickening of the spinal vessels. Vascu lar malformation of the spinal cord resulting in destruction has been de scribed by Brion et al [4] and Antoni [1], The early case reported by Foix and Alajouanine [6] was attributed to localized thrombophlebitis of superficial spinal veins on the anterior aspect of the cord, associated with hemorrhage [15]. A few cases of spinal cord destruction due to ar terial [21] or venous [5] emboli of fibrocartilage originating from her niated discs have been reported.…”

Section: Discussionmentioning

confidence: 99%

Acute Necrotic Myelopathy in Association with Lymphoma Cells of the Reticulo-Endothelial System, Acute Torticollis, and Recurrent Cardiac Arrest

Nishida¹,

Ziegler²

1973

Stereotact Funct Neurosurg

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A case of acute necrotic myelopathy (ANM) is reported in conjunction with a noninvasive reticular type of lymphoma. The clinical course was characterized by two rare phenomena: (1) acute torticollis occurred as an initial manifestation, probably as a result of irritation of the dorsal root or dorsal horn; (2) recurrent cardiac arrest occurred late in the course, probably as a result of hypersensitivity of the sensors of postural change. The occurrence of ANM in patients with neoplasia is reviewed and it is concluded that the nature of the association is unknown. Some evidence points to abnormal immunological reactions leading to vascular damage and cord ischemia.

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Section: Discussionmentioning

confidence: 99%

Acute Necrotic Myelopathy in Association with Lymphoma Cells of the Reticulo-Endothelial System, Acute Torticollis, and Recurrent Cardiac Arrest

Nishida¹,

Ziegler²

1973

Stereotact Funct Neurosurg

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“…Isolated intramedullar vascular malformations are rare [2,4,14,84,121,178,220], while association of extramedullary and intramedullary angiomas is seen in about 20-25% of the cases [59,60,192,224].…”

Section: Location and Major Sitesmentioning

confidence: 99%

“…Often they are considerably thickened due to mural connective tissue proliferation, and severe fibrous or hyalin transformation, with usual lack of any muscular coat ( Figures 7A, 8A, 10A, G, H). Although these vessels do not show elastic lamellae [3], they were called "arterialized" veins [44] or fistulous veins [4]. The same vascular space may show a wall suggestive of an artery along one segment and a venous structure along another, probably representing an AV fistulous communication which, however, is difficult to demonstrate.…”

Section: Morphologic Typesmentioning

confidence: 99%

“…The cord is usually compressed by bulky venous components of large AVMs [94], which also cause damage to the spinal roots ( Figures 7D, E, 10F). Ischemic changes and infarction of the cord are common complications of vascular anomalies [4,26,44,73], which may cause transient attacks [2], "apoplectiform" progression [190,192,214,259] or chronic disease.…”

Section: Complications Of Spinal Angiomasmentioning

confidence: 99%

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Vascular malformations of the central nervous system: A morphological overview

Jellinger

1986

Neurosurg. Rev.

243

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Vascular malformations of the central nervous system (C.N.S.) are classified by size, location, and morphologic type, distinguishing capillary telangiectasias, cavernous malformations, venous angiomas, arteriovenous malformations (AVMs) including varix of the great vein of Galen, and other vascular malformations (e.g. Sturge-Weber syndrome). The morphology and predominant location pattern of the different types of vascular malformations in the brain and spinal cord, and their embryology are reviewed. In the brain and its coverings, all types mainly AVMs and venous angiomas do occur, representing 5-9% of all intracranial space-occupying lesions and 20-40% of the sources of surgically treated intracranial hemorrhages. 50-80% of the angiomas are located in the cerebral hemispheres, 10-18% in central brain areas (basal ganglia, internal capsule, choroid plexus), and 10-30% in the posterior fossa. The major types of cerebral vascular malformations are described with reference to their anatomical features, location, chief arterial and venous supply, and prominent complications. Spinal vascular malformations, accounting for 3 to 12% of spinal space-occupying lesions, include vertebral, extradural, dural, subpial and intramedullary angiomas which occur as isolated or complex vascular anomalies and may involve various covering layers at the same level. The preferential occurrence of angiomas on the dorsal surface of the cord and in the caudal regions is related to the embryologic development of spinal vasculature. Frequent association of spinal angiomas (20-25%) with other vascular anomalies and dysplasias emphasizes their hamartomatous nature and developmental origin. Spinal angiomas include capillary telangiectasias with extra- or intradural and, rarely, intramedullary location, cavernomas, mainly arising in vertebral bodies, venous angiomas, mainly located in vertebral bodies and in the extradural space, and AVMs constituting the commonest type, that may affect both the pial and radicular vessels and can penetrate into the cord. They present as simple AV fistulas, cirsoid angiomas with localized vascular plexuses and large complex convolutions ("juvenile" type). The complications of spinal angiomas include subarachnoid hemorrhage, rare epidural hematoma, hematomyelia, compression lesions of the cord and roots, and ischemic changes causing chronic progressive radiculomyelopathy, previously referred to as Foix-Alajouanine syndrome. Chronic damage to the cord and spinal roots results from pressure effects, thrombosis of the abnormal vessels, disorders of venous drainage, and "steal" phenomena related to the vascular anomalies.

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“…Ischemic necrosis of tissues related to venous anomalies has only occasionally been mentioned in the literature. It is probably the mechanism whereby progressive spinal cord dysfunction occurs in at least some cases that have been designated the "Foix-Alajouanine syndrome," 16 and may well be the mechanism whereby progressive cerebral degeneration occurs in relationship to the predominantly leptomeningeal venous angiomas in the Sturge-Weber syndrome. 17 The analogy of the Sturge-Weber syndrome is further amplified in our case by the fact that the abnormal venous collections were confined to the left hemisphere, corresponding to the lateralization of an unusually dense accumulation of telangiectasias on the left forehead.…”

mentioning

confidence: 99%