Arachnodactyly ("spider fingers") is a medical condition that is characterized by fingers and toes that are abnormally long and slender, in comparison to the palm of the hand and arch of the foot. In some cases, the thumbs of an individual with the condition are pulled inwards towards the palm. This condition is present at birth. Causes
This feature can occur on its own with no underlying health problems, or it can be associated with certain medical conditions, including Marfan syndrome, Ehlers–Danlos syndromes, Loeys–Dietz syndrome, and homocystinuria. It is also seen in congenital contractural arachnodactyly, which is caused by mutation in the gene encoding fibrillin-2 on chromosome 5q23. Notable cases
It remains unconfirmed whether composer Sergei Rachmaninoffs abnormally large reach on a piano was a result of arachnodactyly due to Marfan syndrome, as the pianist exhibited no other signs of the disease.It is also uncertain if blues guitarist and vocalist Robert Johnsons long fingers were attributed to the disease also due to Marfan syndrome. See also
Marfanoid

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Some key differences between EAE in mice, and MS in humans include:

B-cells: Some research points to anti-CD20 B-cells being the basis of the autoimmune attacks. This has been shown to be completely different in EAE and MS.
oxidative injury: Mitochondrial injury is seen in EAE and MS, but mitochondrial gene deletions have so far only been detected in MS lesions. microglia behaviour: In contrast to experimental models of inflammatory demyelination, lesion formation in multiple sclerosis occurs on a background of pro-inflammatory microglia activation, which is seen already in the normal white matter of age-matched controls, and this may contribute to neurodegeneration in the disease. pathological patterns: EAE is unable to reproduce MS pathological patterns III and IV. Secondary damage
Given that some conditions as MS show cortical damage together with the WM damage, there has been interest if this can appear as a secondary damage of the WM. Human Anti-MOG in mice
Anti-MOG associated encephalomyelitis can be passed from humans to mice, inducing MS type II demyelination (pattern II)

Immunogenetic interactions
Deficiency of TBX21 or STAT4 provides resistance against EAE, while interferon-γ-, interferon-γ-receptor-, interleukin-12 subunit α-, interleukin 12 receptor, β 2 subunit-, and interleukin 18-deficiency exacerbated disease. In humans
Sometimes the human equivalent to EAE has been triggered in humans by accident or medical mistake. The reactions have been diverse according to the sources of the disease The researchers in the last report have termed the condition "human autoimmune encephalitis" (HAE).