Myasthenia gravis occurs at all ages, sometimes in association with a thymic tumor or thyrotoxicosis, as well as in rheumatoid arthritis and lupus erythematosus. It is most common in young women with HLA-DR3; if thymoma is associated, older men are more commonly affected. Onset is usually insidious, but the disorder is sometimes unmasked by a coincidental infection that leads to exacerbation of symptoms. Exacerbations may also occur before the menstrual period and during or shortly after pregnancy.
Symptoms are due to a variable degree of block of neuromuscular transmission caused by autoantibodies binding to acetylcholine receptors; these are found in most patients with the disease and have a primary role in reducing the number of functioning acetylcholine receptors.Additionally, cellular immune activity against the receptor is found. Clinically, this leads to weakness; initially powerful movements fatigue readily. The external ocular muscles and certain other cranial muscles, including the masticatory,facial, and pharyngeal muscles, are especially likely to be affected, and the respiratory and limb muscles may also be
involved.

Pathophysiology of myasthenia-At the neuromuscular junction , acetylcholine (ACh) is synthesized in the motor nerve terminal and stored in vesicles (quanta). When an action potential travels down a motor nerve and reaches the nerve terminal, ACh from 150 to 200 vesicles is released and combines with AChRs that are densely packed at the peaks of postsynaptic folds. When ACh combines with the binding sites on the alpha subunits of the AChR, the channel in the AChR opens, permitting the rapid entry of cations, chiefly sodium, which produces depolarization at the end-plate region of the muscle fiber. If the depolarization is sufficiently large, it initiates an action potential that is propagated along the muscle fiber, triggering muscle contraction. This process is rapidly terminated by hydrolysis of ACh by acetylcholinesterase (AChE), which is present within the synaptic folds, and by diffusion of ACh away from the receptor.

In MG, the fundamental defect is a decrease in the number of available ACh receptors at the postsynaptic muscle membrane. In addition, the postsynaptic folds are flattened, or “simplified.” These changes result in decreased efficiency of neuromuscular transmission. Therefore, although ACh is released normally, it produces small end-plate potentials that may fail to trigger muscle action potentials. Failure of transmission at many neuromuscular junctions results in weakness of muscle contraction.

The amount of ACh released per impulse normally declines on repeated activity (termed presynaptic rundown). In the myasthenic patient, the decreased efficiency of neuromuscular transmission combined with the normal rundown results in the activation of fewer and fewer muscle fibers by successive nerve impulses and hence increasing weakness, or myasthenic fatigue. This mechanism also accounts for the decremental response to repetitive nerve stimulation seen on electrodiagnostic testing.

The neuromuscular abnormalities in MG are brought about by an autoimmune response mediated by specific anti-AChR antibodies. The anti-AChR antibodies reduce the number of available AChRs at neuromuscular junctions by three distinct mechanisms: (1) accelerated turnover of AChRs by a mechanism involving cross-linking and rapid endocytosis of the receptors; (2) damage to the postsynaptic muscle membrane by the antibody in collaboration with complement; and (3) blockade of the active site of the AChR, i.e., the site that normally binds ACh.

An immune response to muscle-specific kinase (MuSK), a protein involved in AChR clustering at neuromuscular junctions, can also result in myasthenia gravis, with reduction of AChRs demonstrated experimentally. The pathogenic antibodies are IgG, and are T cell-dependent. Thus, immunotherapeutic strategies directed against either the antibody-producing B cells or helper T cells are effective in this antibody-mediated disease.

How the autoimmune response is initiated and maintained in MG is not completely understood, but the thymus appears to play a role in this process. The thymus is abnormal in 75% of patients with MG; in 65% the thymus is “hyperplastic,” with the presence of active germinal centers detected histologically, though the hyperplastic thymus is not necessarily enlarged. An additional 10% of patients have thymic tumors (thymomas). Muscle-like cells within the thymus (myoid cells), which bear AChRs on their surface, may serve as a source of autoantigen and trigger the autoimmune reaction within the thymus gland.

Role of SUJOK

1.So first step to treat myasthenia is vertical needling on thymus.Sedate He in thymus with magnet stars .In triorigin sedate He in thymus organ,thymys meridian.In six ki also sedate I,II,III IN in L meridian representing thymus.Simultaneous application of all the above 3 theories will bring a dramatic response in 90 percent cases of myasthenia.

2 Give correspondence stimulation on um anahata chakra.

3.In six ki from circulatory system as E to L as immune system(immune system is darkness in 8 ki classification of circulatory system –as per Dr violettas version darkness is just a point so we can only influence darkness only by coldness meridian so liver meridian is functional coldness in type 2 circulation) to again L(as structural wind) as muscles to A(structural dryness) as membrane of muscles to I as receptors on muscle membrane which are getting destroyed u sedate dryness and tone wind,heat and hotness there .Also work on A as membrane of muscles tone heat and sedate dryness there. In acute crisis of myasthenia all the above treatment will shift to yang side.
E-L-L-A-I—–V sedate, . l,ll,lll tone

We have 2 types as immune system —adrenals are kept as dryness in six ki and thymus is kept as darkness in eight ki.Here thymus was main culprit so i choose to prefer immune system as darkness(L meridian) but one can get results by going through A also.This first step was considering functional part of circulatory system so i choose type 2 circulation in my first step of renting but then in subsequent steps as we were entering into structures so i shifted to type 1 circulation where i choose L as muscles,A as membranes and I as receptors.This is how we are able to understand the beauty of type 1 and type 2 circulations invented by Prof.Park.

If the therapist gets confusion in type 1 and type 2 circulation then just work on internal chakras where type 1 and type 2 automatically interchange and there is no need to think which is what.

Sedate He in immune system in triorigin.Give good adrenal,liver and lung ,brain correspondence stimulation.Finally Balance constitution.

4.Dont forget essence of sujok i.e Smile Taichi and SMILE MEDITATION which is a must in patients treatment and his upgradation.ONLY if patient understands that this is just a role given to him by Creator and his role can be upgraded on understanding the concept of Universal Drama he can be cured.