After the short recovery, a lucid period is observed, lasting anywhere from 1 to 4 weeks, in which the patient exhibits no symptoms related to the anoxic episode.
This results in lesions to a great deal of subcortical cerebral white matter but leaves axons, U-fibers, and perivascular myelin mostly untouched.
If it is severe enough, it is known to cause preferential damage to cerebral white matter due to excessive swelling of glial cells while leaving many other tissues unharmed.
The inability to regenerate and remove myelin on certain cells is thought to be responsible for the delay in onset of the disease and for the specificity of the white matter death.
[1][8] Grinker's myelinopathy is diagnosed by establishing a clinical history of carbon monoxide poisoning, narcotic overdose, myocardial infarction, or other global cerebral hypoxic events.
This diagnosis can then be supported by neuroimaging confirmation of broadcast cerebral hemisphere demyelination sparing cerebellar and brainstem tracts.
The neuroimaging evidence can also be used to diagnose Grinker's myelinopathy through an elevation in the concentrations of a myelin basic protein in the cerebrospinal fluid .
[1] Because this disease shares many of the symptoms with various forms of dementia or hysteria, these possibilities must be eliminated before a diagnosis for Grinker's myelinopathy can be made.
Magnetic resonance imaging (MRI) or computed tomography (CT) scans can be used to demonstrate a decrease in white matter density in the patient's cerebral hemispheres, with the typical exception of overlying cortices.
Another preventative measure one can take is to be on bed rest and abstain from stressful and strenuous procedures for the first 10 days after an extended hypoxic event.