Polymicrogyria is characterized by excessive folding of the surface gyri and a thickening of the cerebral cortex, rather than the sulcal scarring that is typical of ulegyria. In addition to morphological differences, the period in which polmicrogyria and ulegyria emerge is also different. Polymicrogyria typically forms while the embryos central nervous system is maturing. Ulegyria is acquired later in development during the perinatal period after neuronal migration has already occurred. It is also suspected that polymicrogyra is genetically linked, whereas ulegyria is caused by environmental factors—namely lack of oxygen.Polymicrogyria can lead to similar conditions that are linked to ulegyria such as mental retardation, cerebral palsy, and epilepsy. It has been observed that patients with polymicrogyria are not receptive to epilepsy surgery. However, responses of patients with ulegyria to similar surgeries are still not fully known, which makes distinction of these two disorders significant. In vivo neuroimaging techniques, namely MRI, have been instrumental in making this distinction. An MRI image of ulegyria is identified by mushroom shaped gyri, deformities in white matter, and localization mainly in the posterior cerebral region. Polymicrogyria is typically recognized by a scalloped appearance at the bordering region between grey and white matter. Although these distinctions have been made with many patients, there is still some difficulty in defining distinct boundaries between these two similar conditions. Detection
Primarily, the main method of detecting ulegyria is through the use of MRI screening for epilepsy. Normally an MRI of an ulegyria affected region will reveal groups of deteriorated neurons with gliosis present.
Amyloidosis is the accumulation on misfolded protein fibers in the body. This is very common condition associated with many of the chronic illness. Haemodialysis-associated amyloidosis is a form of systemic amyloidosis associated with chronic kidney failure. Even if this is common in CKD patients with chronic regular dialysis, it can be also seen in patient with CKD but have never dialysed too. Presentation
Long-term haemodialysis results in a gradual accumulation of β2 microglobulin, a serum protein, in the blood. It accumulates because it is unable to cross the dialysis filter. Affected individuals usually present after 5 years of dialysis rarely before that. The tendency of haemodialysis-associated amyloidosis is to be articular in general affecting the joints. Diagnosis
Prevention
The mainstay of management of the dialysis related amyloidosis is the prevention than the other type of treatment methods. Because most of the medical and surgical managements for this condition may not prevent the symptoms completely. Therefore we have to take adequate precautions to prevent future dialysis disequilibrium syndrome in CKD patients. There are several steps in prevention of dialysis related amyloidosis. Use of high flux dialyzers
Use of Beta 2 globulin absorber
Preserve the residual kidney functions
Early kidney transplant
In addition low copper dialysis is theorized to prevent or delay onset. Management
Management of haemodialysis associated amyloidosis is symptomatic. Although there are lot of methods to prevent and delay the complications, probably the steroids and analgesics may helpful in the management of the condition. However there are some surgical procedure to reduce the pain. See also
Hepatoerythropoietic porphyria
List of cutaneous conditions

References
External links
https://academic.oup.com/ndt/article-pdf/13/suppl_1/58/9896967/130058.pdf