Kathy’s health problems were caused by Multiple Sclerosis disease, but it was not identified during the early stages of her sickness because a thorough disease diagnosis was not performed during her first visit to the hospitals. She claimed to have experienced persistent numbness for a long period especially after waking up and this was a clear manifestation of muscle problems. These symptoms could have helped in predicting Kathy’s problem during the disease onset, which could have led to early diagnosis. Loss of hearing ability was an indication of a serious health problem that could have been identified through prognosis. A precise prognosis could have led to an appropriate medical diagnosis because there are only a few known causes of ear problems. The major causes of ear problems are bacterial infection, physical damage, and obstruction of the Eustachian tubes. Auditory nerve damage is also suspected to cause hearing impairment.
The Ear, Nose, and Throat (ENT) specialist did not suspect impulse transmission to be the possible cause of Kathy’s ear problem, but he instead, reported the absence of pathogenic infections. Fortunately, Kathy regained hearing in her right ear after she was prescribed a high dosage of steroids. It can be concluded that steroids solved Kathy’s problem, although she believed it was a ‘miracle’.
Later on, she was diagnosed with Multiple Sclerosis disease which is known to affect the nervous system. Her loss of hearing ability in the right ear and numbness in the legs occurred due to failure of nerve impulse conduction in the ear region and the leg muscles. The hearing was impaired because skeletal muscles did not receive adequate nervous stimulation required for the initiation of skeletal muscle contractions.
Multiple Sclerosis is an autoimmune disease that affects the nervous system (Peters & Preedy 561). It arises as a result of the improper determination of lymphocytes during the formation of immune cells in the bone marrow. The variant immune cells recognize myelin proteins as ‘foreign’ particles, thus they attack and destroy them. Myelin proteins form the main components of the nerve cell surface. It forms the myelin sheath of the nerve cells and its main role is to determine impulse conduction velocity. Damage to myelin sheath may, therefore, lead to slow impulse conduction as it was observed in Kathy’s case.
Kathy experienced numbness due to two main reasons. The first cause of the symptoms might have been caused by lack of proper nerve impulse conduction in the skeletal muscles and the second cause of her symptoms was due to Copaxone drug side-effects.
Skeletal muscles are involved in the movement of body parts, and contraction of the muscles is regulated by the Somatic Nervous System (SNS) which is coordinated by the spinal cord. Skeletal muscles are organized in a special arrangement to facilitate efficient impulse transduction and muscle activity. Each skeletal muscle consists of the fascicle, muscle fiber, and myofibrils. One fascicle consists of several muscle fibers whereas each muscle fiber is made up of numerous myofibrils. Myofibrils are the main components involved in impulse conduction (Gary 46). They are made up of myosin and actin filaments. These two protein filaments are generally referred to as myofilaments and they serve as the active components of skeletal muscles.
Myofilaments initiate skeletal muscle contraction through several steps depending on the intensity of nerve impulses. The initial step of muscle contraction involves the arrival of an action potential at the synaptic end bulb of the axon terminal. The action potential leads to the opening up of ion channels on the nerve cell membrane hence calcium ions enter into the synaptic bulb through voltage-gated channels. High calcium ions concentration in the synaptic bulb triggers release of acetylcholine by the synaptic vesicles through the exocytosis process. Acetylcholine enters the synaptic cleft where it binds with acetylcholine (ACh) receptors located on the sarcolemma. The binding of acetylcholine to Ach receptors leads to the opening of Na+ ion channels on the synaptic end of the adjacent nerve fiber. Na+ ions move into the cell lumen while K+ ions move from the intracellular region to the outer surface of the cell. The movement of Na+ ions through the nerve cell membrane initiates an action potential along the sarcolemma. The cell’s sarcoma is said to be depolarized when it is in this state, hence the muscle fiber is excited. Action potential initiated on the sarcolemma surface travels along the muscle cell membrane and then enters into the T-tubules, where it triggers the terminal cisternae to release Ca2+ ions into the sarcoplasm. Ca2+ ions bind with troponin leading to shifting of tropomyosin protein, thus exposing the myosin-binding sites which are made up of actin filaments (Gary 47). The power stroke is generated once tropomyosin binds with actin due to the hydrolysis of an ATP molecule leading to the formation of a cross bridge. Subsequent release of ADP by the myosin head causes actin filament to be pulled strongly along myosin until a new ATP molecule binds to the myosin head. Sliding of the actin filament along myosin filament is responsible for skeletal muscle contraction.
Skeletal muscle contractions involve motor neurons that form part of the Somatic Nervous System that innervates skeletal muscles. The speed of muscle contractions depends on the strength of the nerve impulse and the degree of myelination of nerve fibers. Nerve cells with thick myelin sheaths conduct nerve signals at a slow rate, whereas impulse conduction in nerve cells with thin myelin sheaths is normally fast.
Diagnosis of Multiple Sclerosis involves the use of Lumbar puncture and Magnetic Resonance Imaging. Kathy’s problem was identified through these two methods. Cerebrospinal fluid was collected and assayed for the determination of protein levels. An increase of CSF protein levels above the normal range indicates damage in the spinal cord. On the other hand, MRI determines the electrical conductivity of the nerve fibers (Weil 358).
Multiple Sclerosis disease severity has been known to be reduced by steroids because they are made up of essential fatty acids which serve as the building blocks for the formation of the myelin sheath (Peters & Preedy 582). This was the main reason why Kathy’s symptoms subsided after being given a high dosage of steroids by her doctor; although she did not get cured of MS which had caused her hearing impairment.
Kathy’s numbness that occurred before she was diagnosed with MS was due to the destruction of the nervous system, according to the medical interpretation of the initial disease symptoms. Her skeletal muscles could not receive nerve signals from the SNS through motor neurons. However, the numbness she experienced during treatment was due to the side effects of Copaxone. Copaxone’s chemical structure is similar to that of myelin protein, thus it prevents the destruction of the nerve fibers by serving as targets for autoimmune lymphocytes (Olek 169).
Works Cited
Gary, Matthews. Cellular physiology of nerve and muscle, Hoboken: John Wiley & Sons, 2003. Print.
Olek, Michael. Multiple sclerosis: etiology, diagnosis, and new treatment strategies, New York: Humana Press, 2005. Print.
Peters, Timothy and V. Preedy. Skeletal muscle: pathology, diagnosis and management of disease, Cambridge: Cambridge University Press, 2002. Print.
Weil, Andrew. Natural Health, Natural Medicine: The Complete Guide to Wellness and Self-Care for Optimum Health, Boston: Houghton Mifflin Harcourt, 2004. Print.