Neurological Disorders

and number] in format: 12 May 2002] Case Study: The Man Who Began Tripping On The Carpet This case study is to examine the impact that myasthenia gravis disorder has on muscle weakness and what the possible treatments are for this debilitating disease.
The general sequence of events and the molecules involved with respect to nerve stimulation of skeletal muscle cell contraction are
"stimulated by acetylcholine, which is released at neuromuscular junctions by motor neurons. Once the cell are "excited", their sarcoplasmic reticulums will release ionic calcium (Ca2+), this interacts with the myofibrils and, thus, induces muscular contraction (via the sliding filament mechanism). Besides calcium, this process requires adenosine triphosphate (ATP). The ATP is produced by metabolizing creatine phosphate and glycogen, which are stored within the muscle cells. as well by metabolizing glucose and fatty acids, obtained from blood. " (Wikipedia: Skeletal Muscle)
Acetycholine esterase (AChE) "plays an important role in the regulation of functions of central and peripheral nervous systems. AChE hydrolyses the cationic neurotransmitter acetylcholine (ACh)" (Da Ros, 2006).
Curare poison, from the bark of a tree in South America, binds to the ACh receptors but doesn’t activate them. To understand how this works is to think of it described "as a lock and a key ("lock and key model"). The neurotransmitter (the key) fits the receptor site (the lock). Some drugs act just like the key and attach to the receptor site, conveying a signal just like the neurotransmitter (e.g., nicotine). Other chemicals attach themselves to receptor sites but do not convey a message (e.g., the curare poison). This prevents the neurotransmitter itself from conveying the signal and is like a key that fits a lock but does not actually turn the lock, blocking the real key instead." (Palmer, 2003) This is further explained by the following diagram provided by J.K. Palmer at Eastern Kentucky University:
It has been found that organopesticides (OP) bind to acetylcholinesterase and inhibit its normal activity. This will affect muscle tissue by "targeting and depressing acetylcholinesterase activity in a dose-dependent manner, leading to an excessive acetylcholine output, nerve paralysis and finally death. The acetylcholinesterase inhibition is non-specific, affecting the whole body systems via the cholinergic, muscarinic and nicotinic receptor pathways. The body systems affected are the central nervous system, the autonomic nervous system, as well as peripheral muscular pathways" (Tuormaa, T, 2006)
The toxin secreted from the bacterium Clostridium Botulinum, inhibits nerve cell release of acetylcholine and this toxin "affects the body at the neuromuscular junctions called synapses" (Gill, 2004) and "acetylcholine is of paramount importance in any muscle contraction. It is the body’s premier neurotransmitter, a chemical that passes or transmits information from the terminal nerve cell to the target muscle cell across the synapse" (Gill, 2004) As this toxin is the most deadly of all toxins, through the inhibition of the nerve cells for the muscles, it would be safe to say that a person might ultimately be killed through a slow paralysis of the muscles and ultimately, if this toxin was inhaled, for instance, would lead to paralysis of the muscle lining around the lungs which would be the highest probability of death.
Myasthenia gravis is treated through a variety of therapeutic methods. These include:
Medications used to treat the disorder include anticholinesterase agents such as neostigmine and pyridostigmine, which help improve neuromuscular transmission and increase muscle strength. Immunosuppressive drugs such as prednisone, cyclosporine, and azathioprine may also be used. These medications improve muscle strength by suppressing the production of abnormal antibodies. They must be used with careful medical followup because they may cause major side effects.
Thymectomy, the surgical removal of the thymus gland (which often is abnormal in myasthenia gravis patients), reduces symptoms in more than 70 percent of patients without thymoma and may cure some individuals, possibly by re-balancing the immune system. Other therapies used to treat myasthenia gravis include plasmapheresis, a procedure in which abnormal antibodies are removed from the blood, and high-dose intravenous immune globulin, which temporarily modifies the immune system and provides the body with normal antibodies from donated blood. These therapies may be used to help individuals during especially difficult periods of weakness. A neurologist will determine which treatment option is best for each individual depending on the severity of the weakness, which muscles are affected, and the individual’s age and other associated medical problem. (National Institute of Neurological Disorders and Stroke)
As far back as 1934, Dr. Mary Walker successfully used physostigmine which at the time could only be given parentarally and the search for an oral version was found oral prostigmin (mestinon) which has been used successfully every since to treat myasthenia gravis.
In understanding the background of the case is indeed important as it has been found through reading that in many cases, as described on the National Institute of Neurological Disorders and Stroke’s website, that this neurological disorder is often not diagnosed for one to two years from the onset of the disease. This would prove to be most cumbersome I would think for the viewpoint of the sufferer that they are suffering from the disease, but, no physician can provide the exact reason for the symptoms.
There also needs to be more case studies available about the disease as well as more publicity given to this disorder as unless you were looking for information on what a person has now been diagnosed with, a person would not necessarily be privy to how this disease can progress. This can also lead to misdiagnosis by key professionals in an effort to understand the symptoms.
Works Cited
"Skeletal muscle." Wikipedia, The Free Encyclopedia. 22 Feb 2006, .
Da Ros, Tatiana. "Fullerene Derivatives as Acetylcholine Esterase Inhibitors" Pharmaceutical Science Department – University of Trieste, Trieste, Italy. 22 Feb 2006, .
Gill, B.J. "The Botox Lowdown: Science, Safety and Success". Illumin. USC Viterbi, School of Engineering. 23 Feb 2006, Tuormaa, Tuula E. "The Adverse Affects of Agrochemicals on Reproductive Health". FORESIGHT, the Association for the Promotion of Preconceptual Care. 23 Feb 2006,