The main cause of the neurological disorders is believed to be demyelination of the cerebral hemispheres, though there is currently no widely accepted consensus on why. The most commonly accepted theories for the cause of demyelination include hypoxia and cerebral edema due to carbon monoxide toxicity, drug overdose, or cerebral blood vessel damage, and a disruption of myelin-producing pathways. Carbon monoxide toxicity Because carbon monoxide binds to hemoglobin more efficiently than oxygen and lower systemic blood pressure brought upon by an acute anoxic episode in conjunction with carbon monoxide poisoning often leads to cerebral ischemia, a condition where the brain does not receive enough oxygen to satisfy its needs. This results in lesions to a great deal of subcortical cerebral white matter but leaves axons, U-fibers, and perivascular myelin mostly untouched. Support against this theory stems from the ability to replicate these lesions by using nitrogen-induced hypoxia and hypotension in cats and the onset of this disease in individuals who experienced acute hypoxia without carbon monoxide poisoning Cerebral edema Cerebral edema, or unusual swelling of the brain, is commonly caused by anoxic episodes. 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. This theory suggests that hypoxia and carbon monoxide induce a form of edema resulting in white matter necrosis. Evidence for this theory comes from the observation of pathological lesions mimicking those of carbon monoxide poisoning where hypoxia and dehydration along with too-rapid rehydration have taken place without carbon monoxide present. Disruption of myelin-creating pathways The anoxic event is likely to cause damage to cytoplasmic ATP-dependent enzymes in oligodendrocytes. Because many of these enzymes play essential roles in myelin turnover, damage to these enzymes is thought to adversely affect the ability of the body to sustain myelin in white matter, leading to the demyelination of those areas of the brain. 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.
Grinker myelinopathy
Diffuse myelinoclastic sclerosis
Neuromyelitis optica spectrum disorder
Cerebrotendineous xanthomatosis
Akureyri disease
Fasciolopsiasis
White dot syndromes
Camel spongiform encephalopathy