Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[A case of simultaneous medullary hemorrhage and hematomyelia]. 1065 65

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.
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PMID:Hematomyelia caused by ruptured intramedullary spinal artery aneurysm associated with extramedullary spinal arteriovenous fistula--case report. 1752 52

Spinal arteriovenous malformations are rare in children, although perimedullary arteriovenous fistulas (PMAVFs) may account for up to 24% of spinal arteriovenous malformations in this age group. Reported presentations of PMAVFs have included progressive or acute myelopathic symptoms, pain, hematomyelia, and subarachnoid hemorrhage. No known reports of an unruptured PMAVF causing communicating hydrocephalus have been previously published. A 17-month-old girl presented to the authors' clinic with a 6-month history of back and leg pain, gait regression, constipation, and marked lumbar hyperlordosis due to a PMAVF. A brain MRI study also demonstrated advanced hydrocephalus. The patient underwent embolization with Onyx of 2 feeding arteries from the right L-1 and 1 feeding artery from the left L-1 lumbar arteries. Postembolization follow-up imaging demonstrated a reduction in size of the L-1 pedicles and no residual supply of the fistula. Three-year clinical follow-up showed normal bowel and bladder function with significant improvements in the patient's back pain, gait, and hyperlordosis. The patient's ventricular enlargement improved without direct management of her hydrocephalus. To the authors' knowledge, this is the first reported case of communicating hydrocephalus caused by an unruptured PMAVF. The authors postulate that the origin of hydrocephalus was either central venous hypertension caused by the high-flow fistula or a change in fluid dynamics reducing CSF resorption through arachnoid granulations in the lumbar region of the spinal cord. The exact role that spinal arachnoid granulations play in CSF resorption is not currently known. Regardless of pathogenesis, initial treatment should focus on management of the fistula with additional hydrocephalus management only when necessary.
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PMID:Communicating hydrocephalus caused by an unruptured perimedullary arteriovenous fistula in the lumbar region of an infant. 2324 Aug 50

Spinal epidural arteriovenous fistulas with perimedullary venous drainage cause venous hypertension, and usually manifest as slowly progressive myelopathy. We treated two patients presenting with sudden onset of severe neurological deficits. Moreover, in Case 1, the venous drainage was exclusively epidural and no perimedullary venous drainage was present. Angiographic findings of this patient were characterized by a slow-flow fistula with marked retention of the epidural venous drainage. Rapidly progressing thrombosis of the epidural venous plexus may have caused the sudden onset of the symptoms. In Case 2, hematomyelia may also be possibly associated with the sudden onset of the symptoms. Early diagnosis and treatment are essential to achieve favorable outcome in such cases because venous congestion results in irreversible venous infarction within a short period.
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PMID:Spinal epidural arteriovenous fistulas with unusual manifestation of sudden onset of severe neurological deficits: case report. 2409 87