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)

A 47-year-old woman was admitted to our hospital with a giant spinal arteriovenous malformation (AVM) causing heart failure and thoracic myelopathy. Angiography revealed that the spinal AVM had multiple feeding vessels branching from the 5th through 12th intercostal arteries. The drainage vein flowed to the azygos vein and superior vena cava. The AVM destroyed the 7th thoracic vertebra. The cardiac output was 16.7l/min and the shunt ratio was 64% before treatment. Embolization with cyanoacrylate was performed because the operation was considered to be associated with a significant risk of paraplegia and organ ischemia. The cardiac output decreased to 11.6l/min and the shunt ratio was reduced to 32%. After embolization the patient demonstrated no symptoms of either heart failure or sensory deficits. During embolization, provocative tests using sodium amytal and lidocaine with magnetic stimulation were also performed. The above findings suggest that provocative tests and magnetic stimulation are useful to predict paraplegia, which could result from embolization while, in addition, embolization is considered to be a useful treatment for multiple shunt and nidus in this region.
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PMID:Successful management of a giant spinal arteriovenous malformation with multiple communications between primitive arterial and venous structures by embolization: report of a case. 888 57

After electrode insertion for epidural spinal cord stimulation, of 625 electrode operations, unexplained, temporary paralysis resulted in 1.8%, and multidermatomal, painful allodynia in 4.2% (of whom 19% had also had temporary paralysis). Diagnostic testing yielded no anatomical explanation. In patients who were awake during operation, these deficits were noted to begin immediately after pain caused by mechanical deformation of the dura. The author hypothesized the following: myelopathy may result from cord ischemia, caused by vasospasm, triggered by pain within or near the spinal canal. The author proposes to prevent these complications by selective epidural anesthesia.
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PMID:Hypothesis about the etiology of unexplained painful myelopathy after minor trauma in the spinal canal. 891 39

Spontaneous spinal epidural haematoma is an unusual but well recognized cause of compressive myelopathy or cauda equina syndrome. Radicular pain is one of the earliest symptoms and a hallmark of spontaneous spinal epidural haematoma, as in the case of cervical spondylosis and disc prolapse. Should an epidural haematoma be located in the cervical spine, the resultant cervical radicular pain may sometimes be erroneously attributed to a cardiac cause, especially in the setting of pre-existing cardiac disease. The error in diagnosis can lead to another pitfall, the addition of heparin. If the etiology of the pain is a cervical epidural haematoma this can have grave consequences. Moreover, patients with cardiac ischemia who are treated with anticoagulants may rarely develop a cervical epidural haematoma. The resulting radicular pain can overlap with cardiac pain and escape recognition. Symptoms of neck and upper extremity pain with bilateral signs of myelopathy with a sensory level should lead to a suspicion of acute cervical cord compression. The addition of heparin can only compound the disastrous consequence of a rapidly expanding spinal epidural haematoma. The following cases illustrate this diagnostic and therapeutic conundrum.
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PMID:Cervical spinal epidural haematoma: the double jeopardy. 894 71

The neurological complications observed in 6 HIV negative intravenous drug users are reported. Four developed acute neuromuscular involvement in a lumbosacral or brachial distribution with rhabdomyolysis, myoglobinuria, hypovolemia, renal and hepatic failure in the 3 most severely affected patients. Despite evidence of immunologic abnormalities and especially presence of anti-heroin antibodies, we feel that causative mechanisms include mixed compression and ischemia with an underlying toxic myopathy, resulting in segmental myopathy with secondary compression of peripheral nerves. Two patients developed myelopathy with acute or chronic onset. The mechanisms were vascular with spinal cord infarction in the acute form and probably infectious with secondary compressive arachnoiditis in the chronic form. In these 2 patients with myelopathy, outcome was poor.
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PMID:[Peripheral nerve and spinal cord complication in intravenous heroin addiction]. 903 43

Diagnosis of myelopathies of vascular origin is difficult and they are probably underdiagnosed at this time because of the lack of diagnostic tools. A recent report of a 58 year old patient who developed ASAS after an episode of cardiac arrest pointed out the importance of MRI and somatosensory evoked potentials (SEP) to support the diagnosis. MRI with T2 weighted imaging demonstrated diffuse signal abnormalities in both gray matter and surrounding white matter below T7. Furthermore, SEP latencies showed a delay between T6 and T7. Therefore, new technologies including MRI and SEP may improve the diagnosis of spinal cord ischemic injuries. A brief discussion of the normal blood supply of the human spinal cord is presented in this review followed by new, pathophysiologically based classifications of the clinical syndromes of vascular myelopathies. A complete description of the clinical syndromes related to vascular myelopathies is included. Vascular myelopathies were divided into acute and chronic syndromes depending on the time at which the pathophysiological events take place. Subsequently, the two major groups of vascular myelopathies were divided depending on the type of vascular damage, e.g., arterial, venous and/or mixed origin. Posttraumatic spinal cord ischemia is included in the present classification because it is generally considered to be a significant factor contributing to secondary damage following blunt trauma. Since several new diagnostic techniques are now available to characterize the pathology of spinal cord injury, physicians involved in the diagnosis and treatment of vascular myelopathies may find the new classification useful in correlating clinical presentation with subjacent pathology. Identification of the correct pathology should result in more accurate treatment approaches.
J Spinal Cord Med 1997 Jan
PMID:Pathophysiological classification of human spinal cord ischemia. 909 61

Five patients with spinal cord infarction underwent electrophysiologic evaluation. Two subjects with complete paralysis had absent compound muscle action potentials (M-responses), suggesting complete loss of lower motoneurons (LMN). Three subjects with incomplete cord infarction had preserved M-responses, reduced voluntary recruitment and abnormally slow motor-unit firing rates during maximal effort, suggesting upper motoneuron (UMN) weakness. These five patients demonstrate a range of neuronal damage after cord ischemia. With severe cord infarction, there is LMN degeneration and paralysis. With partial cord infarction, there is selective interneuron loss, resulting in UMN weakness. Electrodiagnostic evaluation can help determine prognosis for motor recovery after spinal cord infarction.
J Spinal Cord Med 1996 Oct
PMID:Spinal cord infarction: varying degrees of upper and lower motoneuron dysfunction. 923 91

We evaluated transcranial magnetic stimulation producing motor evoked potentials (TMS MEP) as a method to detect spinal cord ischemia during surgery for thoracoabdominal aneurysms. Four groups of swine were subjected to different types of surgically-induced ischemia. TMS MEP and neurological function were assessed at baseline, immediately after the ischemic insult and after four hours of reperfusion/post-ligation. Cross-clamping of the aorta in groups A&B resulted in the disappearance and subsequent reappearance of TMS MEP with significantly prolonged latencies in most animals and variable neurological function. Ligation of intercostal arteries produced no changes in TMS MEP or neurological function (group C). However, after ligation of intercostal and lumbar arteries, group D demonstrated no reappearance of TMS MEP and severe neurological deficits. TMS MEP can provide rapid detection of global spinal cord ischemia and can also predict local devascularization injury.
J Spinal Cord Med 1997 Oct
PMID:Transcranial magnetic stimulation: use of motor evoked potentials in the evaluation of surgically induced spinal cord ischemia. 936 Feb 19

Paraplegia is one of the major complications following repair of aortic aneurysms or congenital malformations and from trauma of the aorta. In a series of 12 surviving patients we describe the clinical features as well as the evolution and pathophysiology of ischaemic lesions of the spinal cord. The clinical characteristics: loss of tendon reflexes, preservation of light touch sensation and bladder function, and the special topography of pin prick impairment, suggest involvement of the central grey matter. This lesion of the grey matter is incomplete in most of the patients and tends to extend for 2-10 segments. In some cases it can extend downward to the conus resulting in complete flaccid paraplegia. On follow-up we have observed limited improvement in most cases. No patient has recovered fully. Except in cases of traumatic laceration, where symptoms existed before surgery, paraplegia followed surgical repair in all other cases. Ischaemia can be related to the duration and the site of crossclamping of the aorta. Clamping above the left subclavian artery and/or a ligation of the intercostal arteries without previous visualisation of the spinal cord arteries can be dangerous. Other factors such as the phenomena of revascularisation and the presence of free radicals are discussed. These could explain delayed postischaemic spinal cord hypoperfusion.
Spinal Cord 1998 Feb
PMID:Ischaemic myelopathy following aortic surgery or traumatic laceration of the aorta. 949 1

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction. Despite advances in diagnosis and surgical treatment, many patients still have severe permanent neurologic deficits caused by this condition. An improved understanding of the pathophysiology of cervical spondylotic myelopathy, particularly at a cellular and molecular level, may allow improved treatments in the future. A detailed review of articles in the literature pertaining to cervical spondylotic myelopathy was supplemented by an analysis of relevant mechanisms of spinal cord injury. The pathologic course of cervical spondylotic myelopathy is characterized by early involvement of the corticospinal tracts and later destruction of anterior horn cells, demyelination of lateral and dorsolateral tracts, and relative preservation of anterior columns. Static and mechanical factors and ischemia are critical to the development of cervical spondylotic myelopathy. Free radical-and cation-mediated cell injury, glutamatergic toxicity, and apoptosis may be of relevance to the pathophysiology of cervical spondylotic myelopathy. To date, research in cervical spondylotic myelopathy has focused exclusively on the role of mechanical factors and ischemia. Fundamental research at a cellular and molecular level, particularly in the areas of glutamatergic toxicity and apoptosis may result in clinically relevant treatments for this condition.
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PMID:A review of the pathophysiology of cervical spondylotic myelopathy with insights for potential novel mechanisms drawn from traumatic spinal cord injury. 987 98

Magnetic resonance imaging (MRI) has become the imaging modality of choice in spinal cord diseases. Computerized tomography (CT) myelography remains a valuable alternative and may be performed even on patients with a known sensitivity to iodine contrast media. Ultrasonography provides excellent intraoperative evaluation of spinal cord injury. MRI, however, offers new knowledge about spinal cord disease, especially in trauma, ischemia and degenerative lesions; using this technique direct visualization of ischemic spinal cord lesions is presently possible. Rare infections or degenerative spinal cord lesions are imaged albeit in a non-specific manner. Cervical and thoracic disk disease may cause severe myelopathy, yet close correlation between images and symptomatology remains mandatory.
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PMID:The spinal cord. 1014 7


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