There is no documented case in the literature of degenerative retinoschisis itself (as opposed to the occasional situation of retinal detachment complicating retinoschisis) in which the splitting of the retina has progressed through the fovea. There is no clinical utility in differentiating between typical and reticular retinoschisis. Degenerative retinoschisis is not known to be a genetically inherited condition. There is always vision loss in the region of the schisis as the sensory retina is separated from the ganglion layer. But as the loss is in the periphery, it goes unnoticed. It is the very rare schisis that encroaches on the macula where retinopexy is then properly used. Hereditary retinoschisis
Hereditary retinoschisis is derived from a defective retinoschisin protein, which is due to an X-linked genetic defect. The genetic form of this disease usually starts during childhood and is called  X-linked Juvenile Retinoschisis (XLRS) or Congenital Retinoschisis. Affected males are usually identified in grade school, but occasionally are identified as young infants. It is estimated that this much less common form of retinoschisis affects one in 5,000 to 25,000 individuals, primarily young males. Schisis is derived from the Greek word meaning splitting, describing the splitting of the retinal layers from each other. However, schisis is a word fragment, and the term retinoschisis should be used, as should the term iridoschisis when describing splitting of the iris. If the retinoschisis involves the macula, then the high-resolution central area of vision used to view detail is lost, and this is one form of macular disease.
Whether these concerns occur in humans is unclear. Elderly
Biophysical studies using NMR spectroscopy has provided molecular details of how inhaled anesthetics interact with three amino acid residues (G29, A30 and I31) of amyloid beta peptide and induce aggregation. This area is important as "some of the commonly used inhaled anesthetics may cause brain damage that accelerates the onset of Alzheimers disease". Physical properties
It is administered as a racemic mixture of (R)- and (S)-optical isomers. Isoflurane has a melting point of 48 - 48.5°Celsius (118 - 119°Fahrenheit) and a boiling point of 48.5 - 49 °C (119 - 120 °F). It is non-combustible but can give off irritable and toxic fumes when exposed to flame. Mechanism of action
Similar to many general anesthetics, the exact mechanism of the action has not been clearly delineated. Isoflurane reduces pain sensitivity (analgesia) and relaxes muscles. Isoflurane likely binds to GABA, glutamate and glycine receptors, but has different effects on each receptor. Isoflurane acts as a positive allosteric modulator of the GABAA receptor in electrophysiology studies of neurons and recombinant receptors. It potentiates glycine receptor activity, which decreases motor function. It inhibits receptor activity in the NMDA glutamate receptor subtypes. Isoflurane inhibits conduction in activated potassium channels. Isoflurane also affects intracellular molecules. It inhibits plasma membrane calcium ATPases (PMCAs) which affects membrane fluidity by hindering the flow of Ca2+ (calcium ions) out across the membrane, this in turn affects neuron depolarization. It binds to the D subunit of ATP synthase and NADH dehydrogenase.