The mechanism of pathogenesis is not known, but is thought to be an autoimmune disorder, similar to<unk> 's thyroiditis, as its name suggests. Consistent with this hypothesis, autoantibodies to alpha-enolase have been found to be associated with<unk> . Since enolase is the penultimate step in glycolysis, if it were inhibited (for example by being bound by autoantibodies), one would expect decreased energy production by each cell, leading to resulting atrophy of the affected organ. This would occur most likely through each cell shrinking in size in response to the energy deficit (and/or in extreme situations from some cells dying via either apoptosis or necrosis, depending on location). This may occur as a result of enough ATP not being available to maintain cellular functions - notably, failure of the Na/K ATPase, resulting in a loss of the gradient to drive the Na/Ca antiporter, which normally keeps out of cells so it does not build to toxic levels that will rupture cell lysosomes leading to apoptosis. An additional feature of a low-energy state is failure to maintain axonal transport via dynein/kinesin ATPases, which in many diseases results in neuronal injury to both the brain and/or periphery. Pathology Very little is known about the pathology of<unk> . Post mortem studies of some individuals have shown lymphocytic vasculitis of venules and veins in the brain stem and a diffuse gliosis involving gray matter more than white matter. As mentioned above, autoantibodies to alpha-enolase associated with<unk>  have thus far been the most hypothesized mechanism of injury.
Hashimoto's encephalopathy
Rasmussen's encephalitis
Japanese encephalitis
La Crosse encephalitis
Saint Louis encephalitis
Powassan encephalitis
Marburg acute multiple sclerosis
Limbic encephalitis