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Traumatic Myasthenia Gravis Lawyer

Our law firm is known for handling even the most complex neurological injury cases resulting from trauma. As this post discusses, we have experience handling a legal case in which Myasthenia Gravis was severely aggravated by an injury.

Myasthenia Gravis comes from the Greek and Latin words meaning “grave muscular weakness.”

Common symptoms of the condition can include:

  • A drooping eyelid
  • Blurred or double vision
  • Slurred speech
  • Difficulty chewing and swallowin
  • Weakness in the arms and legs
  • Chronic muscle fatigue
  • Weakness that comes on with activity, and improves following rest.
  • Difficulty breathing

The most common form of Myasthenia Gravis is an autoimmune condition of the nerve junctions.  The condition causes weakness of the voluntary muscle groups.   The condition is rate (approximately 20 in 100,000 Americans), and few doctors know much about it.  While some doctors will summarily reject the idea that an autoimmune condition can be caused or aggravated by trauma, the tie is now well established in the medical literature.

Why do people with Myasthenia Gravis get weak?  The voluntary muscles of the body are controlled by nerve impulses that arise in the brain. When the nerve impulses from the brain arrive at a nerve ending, it releases a chemical called acetylcholine. Acetylcholine travels across the space (called the neuromuscular junction) to the muscle fiber side, where it attaches to many receptor sites. A muscle contracts when enough of the receptor sites have been activated by acetylcholine. In Myasthenia Gravis, there can be up to an 80% reduction in the number of the receptor sites. The reduction in the number of acetocholine receptor sites is caused by an antibody that destroys or blocks the receptor site.  The autonomic nervous system and the GI tract (which are both known to be injured in traumatic injuries) control the immune system.  Normally the immune system makes antibodies to fight disease.  But, the immune system of the person with Myasthenia Gravis makes antibodies to fight against the receptor sites of the neuromuscular junction.  The abnormal function of the autonomic nervous system causes the body to attack itself.  Abnormal antibodies can be measured in the blood of many (but not all) people with MG. The antibodies destroy the receptor sites more rapidly than the body can replace them. Muscle weakness occurs when acetylcholine cannot activate enough receptor sites at the neuromuscular junction to contract the muscle normally.

This can progress to a life threatening state.  A myasthenic crisis occurs when the muscles that control breathing weaken to the point that ventilation is inadequate, creating a medical emergency and requiring a respirator for assisted ventilation. In individuals whose respiratory muscles are weak, the myasthenia crisis can be triggered by infection, fever, or an adverse reaction to medication.

The scientific literature on myasthenia gravis proves that this condition can either be caused, or aggravated both by the trauma of a collision, or the treatment rendered in response to injuries for that trauma. One of the most recent medical text dedicated solely to Myasthenia Gravis notes that of the 23% of Myasthenia Gravis cases which have a known cause 3% are triggered by physical trauma, and another 4% by emotional trauma.  Another article of onset of Myasthenia Gravis after trauma can be found here.

But, the case for aggravation due to trauma and medical treatment for that trauma, is even stronger. Our firm has handled a clear case of traumatic aggravation of myasthenia gravis after an auto accident. In that case, our client was never diagnosed with Myasthenia Gravis prior to the collision, but had slight eye droop symptoms (typically the first sign of MG) 10 years prior to the collision, but with negative lab tests only two years prior to the collision. After a very serious collision between two large vehicles, our client was subjected to a series of treatments known to be aggravating factors for Myasthenia Gravis, including surgery, general anesthetic, morphine, antibiotics, muscle relaxants, and several others. In all, the client had 13 of the 16 known aggravating factors for onset of Myasthenia Gravis as a direct result of the collision, triggering a severe aggravation of the condition. This aggravation took her from having non-symptomatic myasthenia gravis with negative lab tests, to being housebound and having myasthenic crises which required lifetime home care and repeated hospitalizations for a woman who was previously completely healthy and independent. Other cases of post traumatic Myasthenia Gravis have been reported at Johns Hopkins Medical School.

It is because of our experience handling exceptionally complex injury cases that we have become the lawyer of choice for people with traumatic brain injuries, spinal cord injuries, and other serious neurological injuries.  If you have experienced the onset or worsening of Myasthenia Gravis after an injury, and would like to retain an experienced Myasthenia Gravis lawyer to assist you in the matter, either as your primary law firm, or as co-counsel, please contact us at (503) 227-1233.

About the
Author

Aaron DeShaw is a personal injury lawyer at DeShaw Trial Lawyers, a law firm representing injured people with serious injuries including brain injuries and other catastrophic injuries. He has individually, and in association with other law firms, obtained over $1 Billion for his clients. Learn more about Aaron and the Firm.