Infarct spinal

The regenerative medicine and TE fields seem now to have entered a period of positive exploitation of the research base developed over the past several decades, and great expectations are related to the potential shown by these biomedical technologies to treat various pathological conditions such as myocardial infarction, spinal injury, and bone and cartilage defects, among others. Several TE products are in clinical use, and many others are approved or in clinical trials for different tissues. However, also the perfect prototype scaffold, successfully tested in clinics, will not necessarily become a commercial product if the production steps present any difficulty in terms of time, cost, and reproducibihty. Issues in commercial scale-up, quality control, and product distribution still represent barriers to the actual delivery of TE products to ensure commercial success. 

NS AIDs Cyclooxygenases (COX-1, COX-2) l Prostaglandins l Thromboxanes l Sensitization of sensory neurons f Inhibition of spinal neurons Nonselective gastrointestinal ulcers, perforation, bleeding, renal impairment COX-2 thrombosis, myocardial infarction, stroke... 

There have been many sporadic reports that lipo-PGEj is effective in fulminant hepatitis, neuralgia associated with herpes zoster, multiple spinal canal stenosis, cerebral infarction, myocardial infarction, chronic renal failure, and bed sores as well as for its registered indications. 

Venous stasis is slowed blood flow in the deep veins of the legs resulting from damage to venous valves, vessel obstruction, prolonged periods of immobility, or increased blood viscosity. Conditions associated with venous stasis include major medical illness (e.g., heart failure, myocardial infarction), major surgery, paralysis (e.g., stroke, spinal cord injury), polycythemia vera, obesity, or varicose veins. 

Lidocaine is the most widely used local anesthetic. Its excellent therapeutic activity is fast-acting and lasts sufficiently long to make it suitable for practically any clinical use. It stabilizes cell membranes, blocks sodium channels, facilitates the secretion of potassium ions out of the cell, and speeds up the repolarization process in the cell membrane. It is used for terminal infiltration, block, epidural, and spinal anesthesia during operational interventions in dentistry, otolaryngology, obstetrics, and gynecology. It is also used for premature ventricular extrasystole and tachycardia, especially in the acute phase of cardiac infarction. Synonyms for this drug are xylocaine, neflurane, and many others. 

Medullary infarcts can be medial, lateral or combined (Fig. 14.6). The medial territory is supplied by penetrating vessels from the anterior spinal artery and the distal vertebral artery. The lateral territory main arterial supply comes from penetrating arteries from the distal vertebral artery and the posterior inferior cerebellar artery. The small posterior territory is supplied by the posterior spinal artery and the posterior inferior cerebellar artery. Medial... 

Fig. 17.4. Axial T2-weighted images in four patients with acute ischemic myelomalacia of the spinal cord. The hyperin-tense infarctions reflect different lesion patterns depending on occlusion site and collateral supply...

Compared with brain ischemia spinal cord strokes are caused by more diverse etiologies. Up-to-now there is no satisfactory and accepted classification of spinal infarcts. Etiologies include circulatory arterial and venous disorders. From a clinical and pathoanatomical point of view it seems reasonable to differentiate between acute ischemic myelomalacia and subacute to chronic vascular myelopathy (Table 17.1). In most cases MRI enables the differentiation of these two main etiologies. A deficient spinal arterial blood flow generally has various causes, ranging from the occlusion of intercostal or lumbar arteries to affection of the intrinsic arteries of the spinal cord. ... 

Many causes of acute spinal cord infarction (of arterial and venous origin) have been reported (Table 17.2). They include diseases of the aorta and aortic surgery, thromboembolic events and cartilaginous disc embolism, vasculitis, coagulopathy, radiation-induced vasculopathy, toxic effects of contrast medium, epidural anesthesia, periradicu-lar nerve root therapy with crystalline corticoids, decompression illness, shock or cardiac arrest, lumbar artery compression and other etiologies... 

Table 17.2. Causes of acute spinal cord infarction...

In contrast to disc embolism, most patients with thrombotic or embolic infarctions show at least partial recovery in the further course of the disease. Nevertheless, depending on the efforts in diagnostic work-up, the cause of spinal cord ischemia often remains undefined or speculative. 

Cheshire et al. (1996) described 44 patients with spinal cord infarctions. Surprisingly, the mean sen-... 

Moreover, analysis of data coming from greater MR series and our own observations reveal no predominance of infarcts in the upper and mid-thoracic region (Mawad et al. 1990 Weidauer et al. 2002). Thus, the concept of a vulnerable watershed zone at T4 is no longer valid in acute spinal cord ischemia. 

Ischemic infarction of the spinal cord is difficult to establish in the early phase, only 50% of the patients show early demarcation within 24 h. The role of MRI in the acute phase is to exclude hematomyelia, spinal vascular malformation (which requires spinal angiography in special cases) or a compressive lesion. 

In most cases of the thoracolumbar infarction, the swollen cord shows peripheral enhancement of the central gray matter. The concomitant enhancement of the cauda equina was reported first by Friedman and Flanders in 1992 (Fig. 17.8). This phenomenon is a characteristic finding in the course of spinal cord ischemia which might involve the cord itself and the ventral cauda equina as well, which is composed of motor fibre bundles (Amano et al. 1998). It indicates disruption of the blood-cord barrier as well as reactive hyperemia (Friedman and Flanders 1992 Amano et al. 1998). The differential diagnosis of contrast enhancement of the cauda equina includes transverse myelitis, bacterial or viral meningitis, and spinal metastasis. 

If the diagnosis of a compression of a lumbar artery has been established by dynamic spinal DSA showing complete occlusion of the lumbar artery, surgical section of the diaphragmatic crus may prevent irreversible infarction in this rare condition. 

Amano Y, Machida T, Kumazaki T (1998) Spinal cord infarcts with contrast enhancement of the cauda equina two cases. Neuroradiology 40 669-672... 

Berlit P, Klotzsch G, Rother J, Assmus HP, Daffertshofer M, Schwartz A (1992) Spinal cord infarction MRI and MEP findings in three cases. J Spinal Disord 5 212-216 Binkert CA, Kollias SS, Valavanis A (1999) Spinal cord vascular disease characterization with fast three-dimensional contrast-enhanced MR Angiography. Am J Neuroradiol 20 1785-1793... 

Brown E, Virapongse C, and Gregorios JB (1998) MR imaging of cervical spinal cord infarction. J Comput.Assist.Tomogr. 13 (5) 920-922... 

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