Could it be osmotic demyelination?? When the na/k pump slows and intracellular volume increases, blood rushes to the site to try to correct the imbalance. This could be the "short term changes in blood flow" that causes lesions (post w/paper in CCSVI forum). The resulting damage isn't as severe as that seen in typical osmotic demyelination because patients with MS have low potassium and the process of correcting the imbalance is less abrupt...and patients with salt-wasting CAH likely have low Na despite supplementation which also leads to less abrupt correction of imbalance. Treatment for typical osmotic demyelination is done by slowly correcting nutrient deficiencies to avoid causing further demyelination. http://en.wikipedia.org/wiki/Central_po ... elinolysis
Central pontine myelinolysis or CPM for short is a neurological disease caused by severe damage of the myelin sheath of nerve cells in the brainstem, more precisely in the area termed the pons, predominately of iatrogenic etiology. It is characterized by acute paralysis, dysphagia (difficulty swallowing), and dysarthria (difficulty speaking), and other neurological symptoms.
It can also occur outside the pons. The term "osmotic demyelination syndrome" is similar to "central pontine myelinolysis", but also includes areas outside the pons.
Osmotic demyelination in CAH (na/k imbalance in favor of K)http://archneur.jamanetwork.com/article ... qundefined
Finally, magnetic resonance imaging focal areas of T2-increased signal intensity in the white matter, without corresponding to neurological impairment, were detected in 4 (27%) of 15 CAH patients by Sinforiani et al,5 in 14 (36%) of 39 patients by Nass et al,6 and in 7 (30%) of 23 patients by us (R.B., C.L., E.C., C.U., D.F., and V.C., unpublished data, 2003).
In these series, white matter abnormalities were diffuse (mostly periventricular) and focal. Diffuse white matter abnormalities could be an expression of hypotensive episodes, producing infarctions in watershed areas.6 A different explanation could be that they are the expression of myelin sufferance, interpretable as extrapontine myelinolysis, induced by the rapid correction of hyponatremia.6 Concerning focal white matter abnormalities, some of them, such as the lesions in the cerebellum6 and the corpus callosum (R.B., C.L., E.C., C.U., D.F., and V.C., unpublished data, 2003), are similar to those typical of MS.
Connection between osmotic demyelination and dialysishttp://www.ajronline.org/content/182/3/809.full
Osmotic demyelination syndrome is a well-known clinicopathologic entity characterized by edema and demyelination in the pons and extrapontine areas [1–5]. Previous studies have noted the MRI findings of osmotic demyelination syndrome in various patient groups [3, 4]. The pathogenesis of osmotic demyelination syndrome remains unclear, but many underlying diseases are known to be associated with this condition [1, 6, 7]. The syndrome is most often seen after rapid correction of chronic hyponatremia [2, 3, 7, 8], but other diseases that cause fluid and electrolyte disturbances may also lead to myelinolysis [1, 6, 9]. In patients with end-stage renal disease, osmotic demyelination syndrome may develop as a result of the disease itself or because of osmotic changes during hemodialysis [1, 10, 11]. Dysequilibrium syndrome is one of the metabolic complications of hemodialysis that may trigger osmotic demyelination syndrome .http://www.ncbi.nlm.nih.gov/pubmed/2391553
The MRI findings of osmotic demyelination syndrome in patients with end-stage renal disease have not been documented in detail. The aims of this study were to present the brain MRI findings of osmotic demyelination syndrome at the time of an episode after hemodialysis and at follow-up, and to identify possible factors that may contribute to the development of these lesions in patients with end-stage renal disease.
Central pontine myelinolysis and low potassium (alcoholism)
Two patients with chronic alcohol abuse and central pontine myelinolysis are described. One developed a Korsakoff syndrome 2 days before admission to our hospital and the other showed signs of a incipient delirium without Korsakoff syndrome. Diagnosis of incipient central pontine myelinolysis was based on acute brain-stem dysfunction, serum electrolyte disturbances, malnutrition with vitamin B1 (thiamine), B6 (pyridoxine) and B12 (cyanocobalamin) deficiency in combination with typical neuroradiological findings. Hypokalaemia but no disturbance in serum sodium levels was found in both patients. After correction of hypokalaemia and vitamin deficiency the patients showed complete recovery of neurological and neuropsychological function. The findings are interpreted as suggesting that disturbances in serum potassium levels as well as rapid correction of hyponatraemia may be associated with pontine swelling and dysfunction which, if undetected, leads to central pontine myelinolysis.