Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From January 1985 through January 1990, 244 patients (168 males, 76 females, mean age: 69 +/- 14 years) received epidural spinal cord stimulation for the treatment of advanced, nonreconstructable, peripheral vascular disease of the lower limbs due to atherosclerosis in 180 patients, atherosclerosis and/or diabetes in 49, and thromboangiitis obliterans in 15 patients: previous surgery included 101 bypass-grafts in 70 patients, 51% of which below the knee, and 117 sympathectomies in 113 patients as the last resource in face of distal peripheral vascular disease of the lower limbs. Mean ankle-to brachial systolic pressure ratio was .31 +/- .34 on symptomatic limbs; due to pain and advanced disease, walking capacity was assessed in only 151 patients, either on treadmill in 25, or in a metered corridor in 126; angiogram of the lower limbs was performed in every patient unless one not older than three months was readily available; pain at rest was assessed after an analogical scale; partial transcutaneous oxygen tension was measured on the dorsum of the fore-foot of 77 symptomatic limbs (mean: 13.35 +/- 14 mmHg). According to clinical and functional evaluation, 18 patients had exertional ischemia (group I), 87 had permanent ischemia with pain at rest and no tissue loss (group II), and 139 had chronic tissue loss (group III), including 93 ischemic ulcers (mean surface: 3.7 cm2, mean duration: 3.5 months) in 88 patients, 27 limited gangrene, and 24 previous limited non-healing distal amputation. After temporary spinal cord stimulation at T12-L1 level (mean duration: 9 +/- 4 days) with a percutaneous quadripolar electrode lead had allowed for selection of responders, 212 patients received an implantable neurostimulator.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Electric stimulation of the spinal cord in arterial diseases of the legs. A multicenter study of 244 patients]. 143 7

A combined impounder-surface K+ electrode was developed to measure change in K+ ion concentration of the cerebrospinal fluid (CSF) across the dura and arachnoid maters. To determine whether K+ permeability of the rat dura and arachnoid maters is due to an intrinsic permeability, a study was conducted using an atraumatic laminectomy model. Dorsal laminectomy was performed at T7-8, T12, and L1. Artificial CSF containing 4.2 mM, 24.2 mM, or 54.2 mM of K+ was administered by anterograde subdural infusion into the subarachnoid space from the proximal laminectomy site (T7-8), with effluent overflow at the distal laminectomy site (L1). K+ concentration on the dorsal aspect of the central laminectomy site (T12) was measured. It was found that changes in K+ concentrations of the infused solution were detected by the epidural surface electrode. This suggests that the intact rat spinal cord dura and arachnoid maters may be permeable to K+ in this laminectomy model. This study supports the use of the combined impounder-K+ electrode for measuring changes in K+ ion concentration of the CSF that can result from spinal cord trauma and ischemia.
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PMID:Studies on the permeability of potassium ions across the dura and arachnoid mater of the rat spinal cord. 208 21

Hemodynamic responses (blood pressure, as well as cardiac output (CO), peripheral and CNS blood flow changes measured via radioactive microspheres) were analyzed in anesthetized rats 2 min following intrathecal (IT) administration (10 microliters) of either 5-ion control solution or 20 nmol of dynorphin A(1-13) into the lower thoracic space (T10-T12). Mean arterial pressure (MAP) significantly increased within 2 min following IT dynorphin A(1-13) due to rise in total peripheral resistance, whereas CO significantly declined. Two minutes post-IT-dynorphin A(1-13) administration spinal cord blood flow also significantly decreased for 2 cm anterior and 1 cm posterior from the tip of the spinal catheter, which reflected a significant elevation in tissue flow resistance of spinal cord vessels in spite of the reduction of CO. As well, tissue blood flow resistance was also increased at this time in the kidneys and adrenal glands. The results indicate that within 2 min after intrathecal dynorphin A(1-13) administration an acute increase in blood flow resistance of spinal cord vessels around the tip of the spinal catheter occurs, at a time when the animal is also hypertensive. It is suggested that the associated pressor response may, in part, be caused by dynorphin A evoking localized ischemia.
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PMID:Intrathecal dynorphin A administration causes pressor responses in rats associated with an increased resistance to spinal cord blood flow. 256 52

The purpose of this paper is to report a case of medullary ischemia diagnosed by MRI and to determine any MRI characteristics that may be useful for the diagnosis in the light of the published data. The patient was a 60 year-old male with hypertension and diabetes, referred to us for flaccid paraparesis and sphincter disorders of acute onset. Physical examination revealed, beside flaccid paraparesis, both superficial and deep hypoesthesia at L1 level and greater on the right. MRI showed a small area of signal hyperintensity on T2 weighted images and in proton density localized in the posterior part of the spinal cord at the level of T12 body. The patient was treated with oral antidiabetic, antiaggregant and antihypertensive drugs as well as neuromotor rehabilitation, and his clinical conditions improved; a control MRI, six months later, showed disappearance of the previous finding and only mild medullary atrophy at the level of the lesion. Medullary ischemia has been observed in a variety of pathological conditions (inflammatory, neoplastic, traumatic degenerative and iatrogenic), and most frequently involves the dorsal portion of the spinal cord. Four clinical-pathological manifestations of medullary ischemia have been described: infarction from occlusion of the anterior spinal artery; "patchy" or "lacunae infarction"; "transverse ischemic infarction"; selective ischemia in the regions of the posterior spinal arteries. A review of the literature yielded 61 cases of spinal ischemia diagnosed by MRI for a total number of 80 MRI scans, 12 of which were long-term controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spinal cord ischemia diagnosed by MRI. Case report and review of the literature. 762 69

We have presented a patient (48 year-old male) in whom the evoked spinal potential monitor detected impending spinal ischemia after aortic cross-clamping, which allowed surgical intervention to be modified so as to restore the decaying evoked spinal potential. The patient received replacement of the dissecting aneurysm in the thoracic descending aorta with clamping of the aorta at the sites immediately proximal and distal to the aneurysm and initiation of femoro-femoral venoarterial bypass under normothermia. The evoked spinal potential was recorded via the T12/L1 epidural electrode in response to transdural electric stimulation of the spinal cord at the C7/T1 level. As the evoked spinal potential gradually decreased in amplitude without latency prolongation after aortic cross-clamping, the distal clamp was moved from the T6 vertebral level to the T4. The reduced spinal potential then returned to the baseline amplitude. This episode was repeated twice from surgical necessity. The patient was free from any neurological disorders postoperatively.
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PMID:Safety management of a patient undergoing thoracic aortic surgery by spinal evoked potential monitoring. 949 6

We have previously demonstrated the importance of activated neutrophils in compression-induced spinal cord injury (SCI) in rats. In the present study, we investigate the action of neutrophil elastase in posttraumatic SCI, using two neutrophil elastase inhibitors (Eglin C and L658,758). SCI was induced by applying a 20-g weight to the spinal cord for 20 min at the level of T12, resulting in hindlimbs motor disturbances, which, when evaluated using a inclined-plane test, were significantly attenuated by Eglin C or L658,758. Histologic examination revealed that intramedullary hemorrhages observed 24 h after trauma were markedly attenuated in these agents. These inhibitors also significantly decreased neutrophil accumulation as shown by myeloperoxidase activity in the damaged spinal cord segment. Induction of leukocytopenia had the same effects as Eglin C or L658,758. These findings implicated neutrophil elastase in SCI. The enzyme may induce vascular damage leading to spinal cord ischemia.
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PMID:Role of neutrophil elastase in compression-induced spinal cord injury in rats. 967 7

Stress proteins are assumed to protect cells against various kinds of stresses including ischemia. In this study, we focused on the behaviour of the most abundant myocardial stress protein, alpha B-crystallin, during ischemia and reperfusion of the pig heart in vivo, alpha B-crystallin constitutes 1-2% of the soluble protein pool and underwent, during severe but reversibly damaging ischemia (25 min), complete translocation to the Z-line area of myofibrils. Irreversibly damaging ischemia (60 min) was accompanied by extreme stretching of the majority of myofibrils, and by concomitant extension of alpha B-crystallin localization from the Z-line area to I-bands. This I-band shift correlated with displacement of the T12 epitope of titin from the vicinity of Z-lines into I-bands, indicating that the primary binding sites for alpha B-crystallin might also be located in juxtaposition to Z-lines and move into the I-bands during extreme sarcomeric stretching. During reperfusion after 25 min of ischemia, alpha B-crystallin disappeared rapidly from myofibrils: whereas reperfusion after irreversibly damaging ischemia (60 min) resulted in dissociation of alpha B-crystallin only from those myofibrils and myocardiocytes that were still able to contract, and alpha B-crystallin remained bound to the overstretched, damaged myofibrils no longer capable of contraction. The time course of translocation of alpha B-crystallin to myofibrils during ischemia correlated with phosphorylation of approximately 20% of the entire alpha B-crystallin pool. However, disappearance of alpha B-crystallin from myofibrils during reperfusion was not accompanied by dephosphorylation, indicating that phosphorylation alone does not explain myofibrillar binding of alpha B-crystallin. Ischemia-induced myofibrillar targeting of alpha B-crystallin probably requires additional structural and posttranslational modifications of myofibrillar components in juxtaposition to I-bands.
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PMID:Binding of the stress protein alpha B-crystallin to cardiac myofibrils correlates with the degree of myocardial damage during ischemia/reperfusion in vivo. 1019 88

A 30-year-old healthy woman was involved in a road traffic accident. She sustained a fracture dislocation of T11/12 with a complete Frankel A paraplegia below T11. She had no associated injuries. High Dose Methylprednisolone was administered according to the NASCIS III protocol (48 h) together with low molecular weight Heparin and gastroprotected medication. Complete transection of the spinal cord and an anterior haematoma from T11 to T12 were confirmed on X rays, CT's and MRI scans. Posterior surgical stabilisation was performed using Isola instrumentation, starting 8 h post injury. Her post surgical period was uneventful except for some episodes of low blood pressure (85/60 mmHg) from which she had no symptoms. On the 12th post operative day, while in the physiotherapy department, she complained of right scapular pain. This occurred every time she was sat up and was associated with paraesthesia of both upper limbs. Two days later she deteriorated neurologically and her level ascended initially to T8 and then to T3. MRI of the spine with and without gadolinium showed spinal cord oedema between C3 and T1. There was no evidence of haemorrhage or syringomyelia. The authors discussed this case making different hypotheses. They are mainly the following: (1) Gradually ascending ischaemia due to a vascular disorder; (2) Double spinal trauma; (3) Ischaemia related to repeated hypotensive episodes; (4) Low grade intramedullary tumour; and (5) Thrombus of the Radicularis Magna artery. The case has been recognised as being very rare and interesting. In the conclusions, the presenting author stresses the importance of adopting MRI-compatible instrumentation for the surgical stabilisation of the spine, and careful monitoring of blood pressure during the acute phase of spinal cord injury. Dr Aito agrees with Mr El Masry about the opportunity of forming a group of clinicians in order to discuss protocols to cope with this devastating complication.
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PMID:Ascending myelopathy in the early stage of spinal cord injury. 1049 Aug 52

This is the fourth in a series of articles on the spine. The first reviewed the anatomy of the neck; the second reviewed the upper thoracic spine and chest (T1-T4); and the third reviewed the middle thoracic spine and chest (T5-T8). The procedures performed in the lower thoracic spine include percutaneous biopsies of the liver and kidneys, percutaneous nephrolithotomy, spinal injections, radiofrequency ablations, electromyography of the diaphragm, trigger point injections, chemodenervation with botulinum toxin, acupuncture, aneurysm repair, and, occasionally, chest tube placement in the lower lung fields. Complications include subcapsular hematomas, infections, pneumothorax, hemothorax, spinal cord ischemia and resultant paraplegia, and, rarely, nephropleural fistulas. This article provides anatomically accurate schematics of innervations of the lower thoracic chest and spine (T9-T12) that can be used to interpret the magnetic resonance images of the muscles and the nerves. Cross-sectional schematics of the lower thoracic chest and spine were drawn as they appear on imaging projections. The relevant nerves were color coded. The muscles and skin surfaces were labeled and assigned the color of the appropriate nerves. An organized comprehensive map of the motor innervation of the lower thoracic chest and spine allows the physician to increase the accuracy and the efficacy of interventional procedures. This could also assist the electromyographer in correlating the clinical and electrophysiological findings with magnetic resonance images.
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PMID:Sectional neuroanatomy of the lower thoracic spine and chest. 1725 50

Spinal cord ischemia syndrome (SCIS) is a serious complication which may occur after either internal or surgical diseases in newborn, young children, teenagers and adults; it is also followed by paraplegia. The onset is acute in 95% of cases. In the other cases the onset may be subacute, developing within one week, or it may be chronic, with slow, progressive development, within a few months to a year. The etiology and pathogenesis of this syndrome raises the interest of many medical fields, such as anatomy, physiology, internal medicine, surgical and imaging specialties. In current medical practice the role of spinal arteriography in diagnosing spinal cord ischemia is essential. Arteriography reveals obstructive lesions in the emerging area of the lumber artery, located between T8 and T12 in 85% of patients. Usually, after diagnosing this syndrome, it may be very difficult to reveal the underlying disease and it may require several investigations such as normal and 3D CT scans, SCIS, cerebral or myelic densitometries. This condition may be caused by metabolic congenital or acquired diseases, infectious vascular diseases, osteoporosis: it may also occur after general or peridural anaesthesia or surgical procedures such as spine surgery, neuro- and cardio-vascular surgery, vertebral and myelic trauma and so on. Treatment for this syndrome will be conducted with respect to the underlying disease. Prognosis may depend on patient's age and it is usually difficult to estimate due to the impossibility of determining the type and extent of the medullary lesion (axonotmesis, neurotmesis or other lesions).
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PMID:Current opinions regarding the spinal cord ischemia syndrome. 1838 2


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