Treatment
Many doctors commonly recommend a combined treatment of a warm compress applied to the eyes (to relieve muscle tension, relax the muscles, and reduce swelling), a small dosage of antihistamine (to reduce any swelling that may be caused by an allergic reaction), increased bed rest and decreased exposure to computer screens, televisions, and harsh lighting (to allow muscles to rest), and monitoring caffeine intake (as too much caffeine can cause an adverse reaction such as eye twitching, but a controlled dose can serve as an effective treatment by increasing blood flow). Etymology
The term comes from the Greek -mŷs – "muscle," + kŷm, -kŷmia – "something swollen" or -kŷmos – "wave"). See also
Blepharospasm
Carnitine palmitoyltransferase II deficiency
Fasciculation
Myoclonic jerk (myoclonus)

References


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History
AMAN, also known as Chinese Paralytic Syndrome, was first described by a group of Johns Hopkins University and University of Pennsylvania neurologists in collaboration with neurologists from the Second Teaching Hospital of Hebei Medical School and Beijing Childrens Hospital. In 1991, Guy Mckhann, Jack Griffin, Dave Cornblath and Tony Ho from Johns Hopkins University and Arthur Asbury from University of Pennsylvania visited China to study a mysterious epidemic of paralytic syndrome occurring in northern China. Every summer, hundreds of children from rural China developed acute paralysis and respiratory failure. Hospitals were overwhelmed with number of cases and often ran out of ventilators and hospital beds. Examination of these children showed that many of them had acute flaccid paralysis and areflexia but with little or no sensory loss. Electrophysiological testing of these children showed motor axonal loss with occasional conduction block with a lack of demyelinating features and normal sensory potentials. In contrast, the common form of Guillain–Barré syndrome in the West often presents with sensory loss and demyelination on electrophysiology testing and is more common in adults. Later, several autopsies confirmed the focus of the immune attack was at the motor axolemma especially around the nodes of Ranvier. These cases showed deposition of antibody and complement along the motor axolemma and associated macrophage infiltration. References


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