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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemia of the motoneurons in the anterior horn is a well known pathological entity. Their clinical signs and symptoms are similar to those of amyotrophic lateral sclerosis. Evidence by selective angiography of angiomas of the spinal cord or compression or deviation of Adamkiewicz artery may be suggestive of an initial vascular lesion. Various data (knowledge of development or lesions during experimental ischemia, selective electrophysiologic analysis of anterior horn neurons, evidence of precise circumstances of spinal vascular disorder or spinal arteriography) suggest that anterior horn ischemia is a multiple aspect phenomenon. Our 4 cases illustrate this hypothesis and demonstrate under confirmed vascular circumstances the different clinical aspects of anterior horn ischemic lesions. In addition to typical amyotrophic paralysis unusual or misleading symptoms may occur such as claudication, paroxysmal contractures or progressive spastic paraparesis. Investigations required and possible treatment of the lesions are simplified by awareness of these various clinical aspects.
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PMID:[Ischemia of the anterior horn of the spinal cord]. 264 83

The danger of irreversible ischemic damage to the spinal cord following repair of traumatic aortic rupture has prompted many techniques designed to decrease this risk. Surgical repair was performed on 41 consecutive patients, using four different methods. These included: group 1 (15 patients), left-heart pump bypass with systemic administration of heparin; group 2 (7 patients), heparinized shunt from the ascending aorta to the descending aorta or to the femoral artery; group 3 (14 patients), heparinized shunt from the left ventricle to the aorta or femoral artery; group 4 (5 patients), aortic cross-clamp only. Spinal cord ischemia was not seen in groups 1 or 2, but paraparesis or paraplegia developed in 4 patients in group 3. Severe shock accompanied rupture in all patients in group 4, and no time was taken for a shunt or bypass. Four of the 7 deaths occurred in the operating room in patients who had arrived moribund and in severe shock. In our experience, shunts from the left ventricle to the aorta have failed to protect the spinal cord against ischemia. Left-heart bypass or aorta-to-aorta shunts are now our procedure of choice.
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PMID:Spinal cord ischemia following operation for traumatic aortic transection. 376 13

Management of dissections of the descending thoracic aorta remains controversial, especially with regard to timing and method of repair. To clarify these and other issues we have reviewed our total experience with repair of descending aortic dissections between 1962 and 1983. The 44 men and 20 women had a mean (+/- SEM) age of 59 +/- 2 years (range, 19 to 83 years), and in all patients the dissection originated in and was limited to the aorta distal to the left carotid artery (Stanford type B, DeBakey types IIIa and IIIb). Twenty-nine patients underwent operation within 2 weeks of the onset of symptoms (acute), and the remainder had later repair (chronic). During repair, circulation distal to the aortic cross-clamp was supported with cardiopulmonary bypass or shunt in two thirds of patients. Overall, 18 deaths occurred less than or equal to 30 days postoperatively (operative risk 28%), and risk was higher in acute (45%) than in chronic (14%) dissections. Operative risk was not significantly related to protection of the distal circulation. The most serious postoperative complication was spinal cord ischemia manifested by paraplegia in five patients (8%) and transient or permanent paraparesis in six patients (9%). Risk of spinal cord ischemia was significantly lower in patients who had protection of the distal circulation during operative repair (8% vs. 44%, p = 0.003). Late survival, including hospital deaths, was 49% +/- 7% at 5 years after operation; 22 of the 46 patients who survived repair were found to have aneurysms involving the thoracic and/or abdominal segments of the aorta. Our results indicate that repair of chronic dissection of the thoracic aorta has a lower operative risk than repair of acute dissections, and initial medical management of acute dissection may be indicated if no early complications occur. Risk of spinal cord ischemia is significantly reduced by cardiopulmonary bypass or shunt and is preferred over aortic cross-clamping alone. Finally, these patients require careful long-term follow-up because of the high incidence of residual or recurrent aortic aneurysms.
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PMID:Early and late results following repair of dissections of the descending thoracic aorta. 394 28

This report describes a patient with Paget disease of the lower thoracic and lumbosacral vertebrae who developed slowly progressive paraparesis. The electromyographic findings were abnormal in the thoracolumbar paraspinal muscles and the right medial gastrocnemius muscle. In the presence of a normal myelogram, we concluded that the denervation found by electromyography was due to neural ischemia rather than mechanical compression of neural tissue, as is sometimes the case.
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PMID:Electromyographic abnormalities in Paget disease of the thoracolumbar vertebral column. 724 63

Metabolic alterations after experimental contusion injury of the spinal cord were evaluated by determining qualitative spinal cord glucose utilization (SCGU), SCGU was determined by the 2-deoxy-D-[14C] glucose technique. An increase in SCGU occurred at the site of maximal impact in the white matter after an injury causing paraparesis and in near trauma regions after an injury causing either paraparesis or paraplegia. These findings are most likely due to anaerobic glycolysis resulting from a reduction in blood flow that still allows delivery of substrate to tissue. Although an initial increase was observed at the site of maximal impact after a paraplegia-causing injury, SCGU in the white matter demonstrated a progressive deterioration by 4 and 8 hours after injury. A failure of substrate delivery resulting from ischemia is the most likely cause for this reduction in SCGU. The somatosensory evoked potential was found to be a very sensitive indicator of the remaining functional axons at the injury site.
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PMID:Spinal cord glucose utilization after experimental spinal cord injury. 727 71

Numerous investigators endeavored to make clear pathophysiological changes in a traumatic spinal cord lesion. The development of neuroscience contributed to have an influence on methods of these researches. This study was undertaken to assess electrophysiological changes resulting from variable periods of experimental spinal cord compression or ischemia by using the evoked spinal cord potentials. Experiments were performed on dogs. Following laminectomies at Th7-9 and L3-4 levels under anesthesia, cord injuries were produced at the lower thoracic level by inflation of an extradurally placed balloon which produced slow graded compression of cord dorsum. Evoked spinal cord potentials to sciatic nerve stimulation were recorded from bipolar electrodes in the midline dorsal subdural space at the operative sites. The normal wave forms of two responses consisted of initially positive triphasic potentials (P1, N1, P2). The conduction velocity of the ascending afferent from the leg was found on the average to be 54.8 +/- 9.7 m/sec between lumbar and dorsal cord. On the basis of the conduction velocities and the responses to stimulus intensities, the afferent volley recorded in the present experiments might reflect synaptic cord afferent pathways originated without Group I fibers in the cord dorsum which were situated ipsilateral to the stimulated nerve. After inflation of the balloon with 0.1 cc of water, spinal canal narrowing rate increased to 14.3 +/- 2.9%. The evoked spinal cord potentials in the lead rostral to the site of compression began to decrease in amplitude. When more water was added into the balloon up to 0.4 - 0.6 cc, spinal canal narrowing rate was enhanced to 42.5 - 77.7% in which potentials were abolished. P2 wave was the first to be abolished and subsequently N1, P1 disappeared in order. On the other hand, the potentials reappeared after decompression in the reverse of their disappearance in order. Responses in dogs with complete recovery from paraplegia returned to the precompression wave pattern both in the amplitude and in latency. On the contrary, in dogs with spastic paraparesis, the recovery of wave form was shown as P1, N1 or P1, N1 with depressed P2. Despite this variability, the evoked response from animals with reversible cord injury were discernible in the early period of spinal shock phase. The degree of recovery varied and had no linear relationship to the recovery grade of clinical symptoms. The experimental cord ischemia was made by inflation of a balloon catheter which was inserted from femoral artery into the upper thoracic aorta. The evoked spinal cord potentials were recorded at the midthoracic and lumbar level. Changes of wave form resulting from the ischemic period of 30 minutes were first the amplitude loss of N1 and subsequently that of P2, P1. On the other hand, the responses gradually returned to their pre-ischemic characteristic about 30 minutes after circulatory reestablishment...
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PMID:[Clinical application of the evoked spinal cord potentials. Part 1. Neurophysiological assessment of the evoked spinal cord potentials in experimental cord trauma - with reference to cord compression and ischemia (author's transl)]. 728 22

A 65-year-old male presented with rapidly progressive paraparesis and akinetic mutism due to occlusion of the bihemispheric anterior cerebral artery (ACA). He was treated by intra-arterial thrombolytic therapy but reocclusion of the arteriosclerotic lesion occurred. Bilateral superficial temporal artery (STA)-ACA anastomoses achieved lasting neurological improvement. Bilateral STA-ACA anastomoses are quite effective to prevent ischemia of the bilateral ACA territories.
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PMID:Acute revascularization for bihemispheric anterior cerebral artery thrombosis--case report. 756 79

Aortic replacement for thoraco-abdominal aneurysms remains a major challenge in vascular surgery. Related symptoms, maximal diameter > 6 cm, progression, aneurysm sac containing none or excentric thrombi and uncontrollable hypertension are factors in favour of surgery, if the general condition of the patient allows the operation. Patients with aneurysms < 5 cm maximal diameter, tube-size aneurysms, heavy calcification of the aortic wall, concentric thrombi within the aneurysmal sac and significant cardiopulmonary risks should be treated conservatively. Patients in good general condition with aneurysms around 5 cm maximal diameter should be controlled by computed tomography in 6 to 12 months intervals and in the case of progression surgery can be recommended despite missing symptoms. Crawford developed the 'graft-inclusion-technique', which combines the 'ingraft'-technique with reattachment of renal, visceral and segmental arteries. The 'clamp and repair' principle is used in patients with sufficient cardiac function. Otherwise shunt or left sided heart bypass are used to reduce cardiac afterload. According to the literature local cooling (flush perfusion), cytoprotective drugs and numerous methods to maintain or ameliorate distal aortic perfusion during clamping ischemia have been used in patients successfully for prevention of ischemic spinal complications. In physiological settings these methods may prove valuable, but under pathophysiological conditions of TAAA-repair one must doubt the efficacy, because the individual risk is difficult to assess. In our hands flush perfusion and cooling of the kidneys proved to be helpful. In animal experiments we have shown prolongation of ischemia tolerance time using eicosanoides to protect the kidneys and the spinal cord. If shunt or left-sided heart bypass can protect the spinal cord during clamping, is unknown, because the risk of paraplegia in the individual patient can be known only, if the function of the spinal cord is monitored. We have developed a spinal neuromonitoring system and found, that only one third of all TAAA-patients is at high risk to develop paraplegia during aortic clamping. The surgeon is guided by continuous recording of spinal evoked somatosensory potentials and can adapt the operative technique by early reimplantation and eventually subsequent separate reimplantation of segmental arteries supplying blood to the spinal cord, in order to reduce spinal ischemia time. Our results in 260 TAAA-patients are presented. In a high-risk population of patients with aneurysms type I-III (Crawford's classification) it was possible, to reduce the paraplegia rate from 7 to 3.5%, the risk of paraparesis from 15 to 6%, while the operative mortality was only reduced from 19 to 10%.
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PMID:[Surgical treatment of thoraco-abdominal aneurysm. Indications and results]. 758 56

We report 3 cases of dorsal ischemic myelopathy indicative of aneurysm of the abdominal aorta. In 2 cases the aneurysm was dissecting and in all patients medullary symptoms were preceded by sudden lumbar or abdominal pain. Neurological symptoms were slightly different in each case. One patient experienced 3 episodes of acute paraparesis and rapid regression evoking transitory medullary ischemic accidents (intermittent medullary claudication). Another patient suffered progressive asymmetric paraparesis which first stabilized and later improved partially after surgical treatment of the aneurysm. The third suffered acute paraplegia related to irreversible ischemia of the anterior 2/3 of the medulla. The great variety of clinical manifestations of spinal cord ischemia related to aneurysms of the descending aorta can be explained by the topography of the aneurysm, pecularities of medullary vascularization and, especially, by the diversity of etiopathogenetic mechanisms that give rise to ischemia. We conclude that in the face of symptoms suggesting dorsal ischemic myelopathy, the possibility that an aneurysm of the abdominal aorta may be the cause must be considered, whether or not pain has been experienced prior to signs of medullary involvement.
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PMID:[Spinal cord ischemia indicating aneurysm of the abdominal aorta. Report of three cases]. 761 38

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


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