Spinal ischemia

Adverse effects Severe respiratory depression occurs. Other effects include vomiting, dysphoria, and allergy-enhanced hypotensive effects (Figure 14.4). The elevation of intracranial pressure, particularly in head injury, can be serious. Morphine enhances cerebral and spinal ischemia. In prostatic hypertrophy, morphine may cause acute urinary retention. A serious action is stoppage of... 

Etiology Trauma, viral infections, ischemia, inflammation, genetic defects Neuropathy, genetic defects Peripheral inflammation, peripheral neuropathy, trauma, genetic defects, spinal cord injury, inflammation in the central nervous system ... 

Coles, J., Ahmed, S., Mehta, H. and Kaufman, J.C. (1986). Role of free radical scavenger in protection of spinal cord during ischemia. Ann. Thorac. Surg. 41, 551-556. 

Cuevas, P., Carceller-Benito, F. and Rcimers, D. (1989). Administration of bovine SOD prevents sequelae of spinal cord ischemia in rabbit. Anat. Embryol. 179, 251-255. 

An important methodologic point about the majority of these studies is that they use a reduced preparation, in which the spinal cord is neurally isolated from the brain by a complete transection (129). The rationale for using this simplified preparation is that spinal reflex activity can be analyzed in the absence of supraspinal influences. However, transection may introduce other variables (i.e., ischemia, disruption of the blood-brain barrier, loss of tonic neural activity from supraspinal systems), which may result in drug effects on spinal reflexes that are quantitatively or even qualitatively different than those seen in the intact animal. Thus the following review of hallucinogen effects on spinal reflexes is organized into two main categories (a) studies in transected animals, and (b) those in decerebrate or intact preparations. 

Shohami E, Jacobs TP, Hallenbeck JM, Feuerstein G. 1987. Increased thromboxane A2 and 5-HETE production following spinal cord ischemia in the rabbit. Prostaglandins Leukot Med 28 169-181. 

As previously discussed, the COX-2 inhibitors have selectivity for inhibition of the COX-2 enzyme, which has low constitutive activity but is highly inducible at sites of tissue injury. In addition to the peripheral role of COX-2 in inflammation, COX-2 may play an important role in the CNS. COX-2 is expressed constitutively in some excitatory neurons in the brain and spinal cord and is induced in traumatic brain injury such as that induced by ischemia and seizures. It has been hypothesized that COX-2 may also be involved in neurodegen-erative diseases, since COX-2 inhibitors have shown some positive effects in Alzheimer s disease. Thus, the mechanism of action of COX-2 inhibitors may involve brain and spinal cord sites as well as local sites of injury. 

Noa, et al. Protective effect of D-003 on experimental spinal cord ischemia... 

Kiziltepe U, Turan NN, Han U, Ulus AT, Akar F. 2004. Resveratrol, a red wine polyphenol, protects spinal cord from ischemia-reperfusion injury. J Vase Surg 40 138-145. 

Pavel J., Lukacova N., Marsala J., and MaPala M. (2001). The regional changes of the catalytic NOS activity in the spinal cord of the rabbit after repeated sublethal ischemia. Neurochem. Res. 26 833-839. 

Thiazolidinediones (TZDs) are potent synthetic agonists of PPARy and medicine for type 2 diabetes. TZDs were shown to induce neuroprotection after cerebral ischemia by blocking inflammation (Culman et al., 2007). Spinal cord injury (SCI), another type of neurodegenerative disease, also induces massive inflammation that precipitates secondary neuronal death. Park et al. (2007) analyzed the therapeutic efficacy of TZDs, pioglitazone, and rosiglitazone, after SCI... 

In blockade of the anterior spinal artery, ischemia of the medial medulla may occur with contralateral hemiparesis, ipsilateral tongue weakness and contralateral loss of posterior column sensation (Ho and Meyer 1981). 

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