Central nervous system ischemia

Wieting JM, Dykstra DD, Ruggiero MP, Robbins GB, Galusha K. Central nervous system ischemia after Varicella infection and desmopressin therapy for enuresis. J Am Osteopath Assoc 1997 97(5) 293-5. 

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 ... 

Braughler, M.J., Hall, E.D., Jacobsen, E.J., McCall, J.M. and Means, E.D. (1989). The 21-aminosteroids potent inhibitors of lipid peroxidation for the treatment of central nervous system trauma and ischemia. Drugs Future 14, 143-152. 

Intoxication results in a characteristic intense, throbbing headache, presumably due to cerebral vasodilation, often associated with dizziness and nausea and occasionally with vomiting and abdominal pain. More severe exposure also causes hypotension, flushing, palpitation, low levels of methemoglobinemia, delirium, and depression of the central nervous system. Aggravation of these symptoms after alcohol ingestion has been observed. On repeated exposure, a tolerance to headache develops but is usually lost after a few days without exposure. At times, persistent tachycardia, diastolic hypertension, and reduced pulse pressure have been observed. On rare occasions, a worker may have an attack of angina pectoris a few days after cessation of repeated exposures, a manifestation of cardiac ischemia. Sudden death due to unheralded cardiac arrest has also been reported under these circumstances. ... 

H3-receptors have been identified in the central nervous system. They are located on presynaptic membranes and serve as inhibitory autoreceptors at histaminergic neurons. They are also found on certain human autonomic nerve endings and in atrial tissue where they may inhibit norepinephrine release during ischemia. 

The usual definition of a neuroprotectant is an agent that aims to prevent neuronal death by inhibiting one or more of the pathophysiological steps in the processes that follow injury to the central nervous system (CNS) or ischemia due to occlusion of an artery or hypoxia due to any cause. This definition has now been extended to include protection against neurodegeneration and neurotoxins. The extended definition includes interventions that slows or halts the progression of neuronal degeneration. 

Weisbrot-Lefkowitz M, Reuhl K, Perry B, Chan PH, Inouye M, Mirochnitchenko O (1998) Overexpression of human glutathione peroxidase protects transgenic mice against focal cerebral ischemia/reperfusion damage. Brain Res Mol Brain Res 53 333-338 Wilhams K, Alvarez X, Lackner AA (2001) Central nervous system perivascular cells are immunoregulatory cells that connect the CNS with the peripheral immune system. Gha 36 156-164... 

Ethylene glycol poisoning can canse acidosis, central nervous system depression, pulmonary edema, acute oliguric renal failure with crystalluria, liver damage due to calcium oxalate deposition, nausea, abdominal pain, and cramping, acute colonic ischemia (29), and papilledema and abducens nerve palsy (30). 

Cocaine is a central nervous system stimulant that inhibits the peripheral reuptake of catecholamines, leading to increased sympathomimetic activity [129]. Its abuse is associated with a variety of medical problems. These include acute myocardial infarction, cardiac arrhythmias, cerebrovascular accidents, hyperpyrexia and stimulated sympathetic activity, seizures and coma, obstetrical comphcations, intestinal ischemia and a variety of psychiatric complications [128-131]. A number of reports in the mid to late 1980 s described patients who developed rhabdomyolysis while using cocaine [132-134]. Some of these patients experienced acute kidney injury [135-139]. While the exact incidence of acute kidney injury secondary to cocaine rhabdomyolysis is unknown, in one reported series it occurred... 

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