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Old 04-15-2007, 04:08 PM #1
hsobol4336 hsobol4336 is offline
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hsobol4336 hsobol4336 is offline
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Default Wife of man with intramedullary vascular lesion

Hello everyone:

I am writing about my husband, looking to see whether anyone has any helpful information. My husband is 75 now and although confined to an electric scooter is still working in the education world. His disability started about 25 years years ago with peripheral neuropathy. After many diagnoses were ruled out, including AVM's, Dr. Bennett Stein did a spinal laminectomy, the result of which is the following abstract in the Journal Neurology:


[I]
1: Neurosurgery. 1997 Jun;40(6):1295-301. Links
Unusual intramedullary vascular lesion: report of two cases.
Schwartz TH,
Chang Y,
Stein BM.
Department of Neurological Surgery, Neurological Institute of New York, Columbia-Presbyterian Medical Center, New York, New York, USA.

OBJECTIVE AND IMPORTANCE: Spinal arteriovenous malformations have been divided by location into dural (Type I), intramedullary glomus (Type II), juvenile (Type III), and perimedullary direct arteriovenous fistulae (Type IV). We report two cases of an unusual intramedullary proliferation of hyalinized capillaries that do not fit into any of these categories. CLINICAL PRESENTATION: A 27-year-old woman and a 62-year-old man presented with subacute progressive caudal myelopathy. Magnetic resonance imaging revealed focal spinal cord enlargement, high signal on T2-weighted images, and patchy enhancement with gadolinium consistent with tumor. No serpentine flow voids were visualized on the surface of the spinal cord. Spinal angiography revealed nothing abnormal. No abnormal vasculature was grossly visible on open biopsy. Histological examination of the tissue specimens revealed a proliferation of capillary-sized vessels with varying degrees of vascular wall changes ranging from endothelial hyperplasia to concentric hyalinization, suggesting ongoing evolution of the lesion. Surrounding neural tissue demonstrated ischemic changes characterized by myelin and axonal loss and astrocytosis but no necrosis. INTERVENTION: Patients were treated with chronic anticoagulation, which seemed to slow, but not halt, symptomatic disease progression. CONCLUSION: Although the pathological substrate seems to be an acquired intramedullary vascular lesion characterized primarily by capillary proliferation, the cause of this lesion is unknown. This disease differs from Foix-Alajouanine syndrome and subacute necrotizing myelopathy by an absence of abnormal surface vessels and a lack of intramedullary necrosis. The histological findings are reminiscent of the process that occurs in the kidney and various end organs from long-standing mild to moderate elevations in blood pressure or chronic diabetes. Tissue ischemia may result from luminal obstruction by severe hyalinization and thrombosis. Because the natural history of this disease is unknown, it is unclear whether anticoagulation slowed disease progression.



After the surgery we pretty much gave up on any cure..Now he has Parkinsons as well. At first Sinemet was a great help. Now it puts him to sleep, makes his mouth and tongue go into grotesque movemets and inhibits his speech..Any ideas..
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Old 04-15-2007, 05:16 PM #2
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Jomar Jomar is offline
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Hi,
my dad just had Mirapex ??added about 2 months ago along with the sinemet and it seems to be working very well for him.
He is much more active and has some of his old gumption back.
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