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> CASE 3 Myasthenia Gravis

HB was a career navy man, working as a civilian in the area of logistics management ever since he retired 22 years ago as a chief petty officer. One day two years ago, he noticed his eyes kept drooping as he drove to the navy base. He didn’t think about it again until lunch, when he had to hold his eyes open to see enough to drive home. Concerned, HB went to Urgent Care, where they referred him to a neurologist.

The neurologist ordered blood tests specifically looking for antibodies against acetylcholine receptors and changes in the amount of thymus hormones. Results were positive for the antibodies, confirming a diagnosis of myasthenia gravis, an autoimmune disease. Myasthenia gravis causes the body to attack the receptors for acetylcholine, the main neurotransmitter for motor (muscle) function, causing muscle weakness.

The neurologist treated him with pyridostigmine (Mestinon), a drug that promotes neurotransmitter function by blocking the enzyme acetyl cholinesterase that degrades acetylcholine in the motor end plate. His symptoms resolved quickly, allowing HB to return to work. His neurologist also managed his symptoms with medications that decreased the autoimmune response. His wife searched the Internet and found discussion boards and websites with information on this rare disease, including prognosis and how to cope with the uncertainty. HB was a strong, self-determined man who took these challenges as a sign to live his life to the fullest, so he and his wife began traveling in earnest.

Over the next two years, HB managed his condition with the help of a supportive wife and attentive neurologist. He survived mild episodes of recurrent weakness, each time a little different: discoordinated nasal speech, difficulty swallowing, poor balance. Two months ago, he had to take a break from work due to neck weakness and pronounced difficulty swallowing; he started a course of steroids and hoped the symptoms would resolve. After discussing things with his wife, they cancelled a trip to Machu Picchu so he could rest and try to return to work.

> Neuroplasticity BRAIN Initiative

Understanding the process of neuroplastic change after central nervous system damage allows clinicians to determine the ideal timing and approach for treatment. It is long established that delayed care results in poorer outcomes. However, by identifying the cellular recovery mechanisms, we now understand neuroplastic changes following injury. The damaged system must first reestablish the cell membrane resting potential, and it uses a great deal of energy to restore ionic gradients and repair injured organelles. Any new demands on the healing synapse can potentially hinder recovery. The ideal timing for rehabilitation and activity after stroke remains unanswered. In animal models, introducing exercise too soon after brain injury is shown to hinder hippocampal function, an area essential for learning and memory. Extrapolating these findings to the human brain is an area that should be explored in the near future, due in large part to the efforts ...

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