Inclusion Body Myositis ,or IBM, is one of many muscle diseases known as inflammatory myopathies,

Introduction: According to the “Human Physiology Laboratory Manual “,BIOL 282 ,page 31 , the reason of performing this experiment is to learn how the muscle contraction occurs based on the molecular level and what kind of factors are involved .As a matter of fact, skeletal muscles contain a lot of nuclei because of the cell fusion while being developed and are made of cylindrical cells that have myofibrils. The myofibrils contain sarcomeres and the

Although patients can be preliminarily diagnosed with the syndrome based on an analysis of the physical symptoms, two tests can be used to confirm the diagnosis of GBS. The first is a lumbar puncture, or spinal tap, in order to obtain a small amount of spinal fluid for analysis. The spinal fluid of those with GBS often contains more protein than usual. The second is an electromyogram (EMG), which is an electrical measure of nerve conduction and muscle activity. (3) (4) The symptoms of GBS begin with numbness and tingling in the fingers and toes leading to weakness in the arms, legs, face, and breathing muscles. The weakness begins in the lower portion of the body and rapidly moves upward. This weakness eventually leads to loss of sensation in the affected areas; although a number of cases are mild, temporary limb paralysis is not uncommon. In the milder cases, the numbness can only cause difficulty in walking, "requiring sticks, crutches, or a walking frame." (3) Pain is not uncommon, and abnormal sensations, such as the feeling of "pins-and-needles," can affect both sides of the body equally. Loss

Polymyositis is characterized by progressive muscle weakness that usually starts in those muscles closest to the body’s trunk (i.e. proximal muscles). Other features of the disease may also include difficulty in swallowing and speaking (dysphagia and dysarthria, respectively), shortness of breath, heart beat irregularities and arthritis. In some cases as the disease progresses, the muscles that are furthest away from the trunk of the body (i.e. distal muscles), such as those in the forearms and ankles, may become affected. Furthermore, patients may have other symptoms including but not limited to a low-grade fever and peripheral adenopathy (enlargement of lymph nodes).

Martini, F. H., Nath, J. L., and Bartholomew, E. F. “Muscle Tissue.” Anatomy & Physiology. 9th

Autosomal dominant LGMD occur less often than recessive dominant LGMD. In the metabolism myotilin gene mutations occur, it may be due to a deficiency of vitamin B12, vitamin E, folate or exposures to nitrous oxide. LGMD 1A disease normally occurs from the age 42 to 77, and develops in the same areas (hip, shoulder and back) however, it could spread to the leg muscles. Due to the fact that myotilin gene is mutated, it causes focal myofibrillar destruction to occur, and this results in intracytoplasmic deposits to float around in the blood stream. In one case study done in Barcelona in 2011, there were 13 patients who were all diagnosed with myotilin gene mutation disease. The results showed that the deposits of myofibrillar became immune to myotilin and cluster up the vacuoles and interfere with the Z-lines. Overall the study revealed that each patient shared the same phenotypic characteristics, LGMD 1A and myofibrillar myopathy variations which emphasizes that LGMD is a developing neuromuscular disorder (Montse,

MG may be difficult to diagnose and may not be determined for a couple of years. Reasons are as follows: the onset is gradual with the symptoms worsening over time, weakness and fatigue can also be signs and symptoms of other diseases, one or more of the voluntary muscle groups may experience weakness and with different degrees of severity, and also every patient may experiences the disease differently. After the medical history and physical examination, the physician may see a need for further muscle and neurological tests. Blood tests can detect abnormal antibodies. Nerve conduction studies and repetitive stimulation tests the nerve’s communication with the muscle. When stimulated a number of times the test will indicate muscle weakness. Single-fiber (EMG) electromyography is a test that measures the communication between the nerve and a muscle by inserting a small needle into a single muscle and recording the electrical muscle activity. CT scan or MRI may be ordered to check for

Mild muscle pain can be a common side effect of physical means, such as intense workouts, over usage of muscle, and/or blocked blood vessels, or by chemical means, such as toxins, heat or drugs. Oftentimes, people who experience muscle aches can easily pinpoint the cause due to their knowledge of the stress, tension, or physical activity they have endured. Rhabdomyolysis, or dissolution of skeletal muscle, is a syndrome caused by injury to skeletal muscle and involves the leakage of large quantities of potentially toxic intracellular contents into plasma (Muscal, 2013). In contrast to mild muscle pain, Rhabdomyolysis, commonly known as ‘Rhabdo’, may

Myofascial pain syndrome, otherwise known as MPS, is a chronic pain disorder. The word myofascial broken apart means muscle, and muscle tissue, and fascia which is the membrane supporting muscles. In the condition of MPS, pressure on sensitive points in the muscles, also known as trigger points, cause pain in the muscle. Sometimes the trigger points also send pain to other parts of your body that seem unrelated to the tense muscle, known as referred pain. Myofascial pain syndrome typically occurs after a muscle has been contracted repetitively. Although everyone experiences muscle tension and pain, the discomfort associated with MPS will persist and worsen over time.

The Effects of Different Stretching Techniques on Myosin and Actin Fibers and How it Affects Athletic Performance

Muscular dystrophy can be diagnosed with a physical exam and diagnostic testing completed by the child’s pediatrician. Additional information that will be obtained during the examination will be family history, pregnancy history, and birth history. Diagnostic studies for muscular dystrophy include muscle serum enzymes (especially creatine kinase), electromyogram (EMG) testing, muscle fiber biopsy, electrocardiogram abnormalities reflective of cardiomyopathy, and genetic pedigree (Lewis, 2011). Duchenne muscular dystrophy is caused by the lack of dystrophin. A muscle biopsy can be done to confirm a diagnosis of muscle dystrophy. The biopsy will show evidence of significant fat and connective tissue deposits, deterioration and necrosis of muscle fibers, and a lack of the muscle

Manual muscle testing will be tested to assess the strength in muscles used for running such as the prime/strong muscles which are the hamstrings, gastrocnemius, soleus, quadriceps, and tibialis anterior. This will also determine the weakness in muscles such as the plantarflexors, dorsiflexors, knee flexion, and knee extension. Also, range of motion will be tested on the tight muscles such as the hamstrings, gastrocnemius, quadriceps, and tibialis anterior. When the muscles are tight, the runner will increase the risk of injury (Schipper, 2009). Gait analysis will be used to examine deficits to body function, stability, and describe how the patient will be running. This will help determine the patient’s biomechanics and achieve adequate mobility. Lastly, we will perform a pain assessment to see what pain level the patient is at when running. This will help determine whether the patient is minimizing stress on the body to achieve no pain at all while running. To monitor progress of these assessments, we must know that if these “muscles are weak or become fatigued easily, there is less control of the leg and the risk of injury increases" (Schipper, 2009, paragraph

Goals of Treatment Plan include decreasing pain/spasms, increasing range of motion/ability to perform normal activities of daily living/strength, returning the patient to his pre-clinical status and increasing function. Long term goals include the reduced usage of over-the-counter/prescription medications as well as an increase in up to 5-10 repetitions of therapeutic exercise/neuromuscular education and an increase in 2-5 minutes of spinal endurance exercises (recumbent bike/ergometer) by the next

What patients experience due to this disease are a range of physical and cognitive problems. According to Bonafede (2013), these symptoms may include difficulty with balance, muscle coordination, memory, concentration, vision and speech. Moreover, they may “come and go or become progressively worse,” which will end up hindering the person’s abilities and productivity. Until recently, the major course of therapy only included the use of steroids, due to their immunosuppressive qualities; however, now “several new compounds have been developed and approved,” in hopes to change the course of the disease (Tavazzi, 2014, 833). Current available treatments include steroids and Glatiramer acetate, Natalizumab, and Fingolimod. The first, suppresses the immune system to reduce the inflammatory response, thus avoiding the immune cells from entering the central nervous system. However, long-term use of steroids puts the patient at risk for infection or hypertension; so, during the use of these drugs one must make into account if the benefits outweigh the risk. The latter, is a “synthetic amino acid polymer resembling myelin basic protein,” delivered via injection (Tavazzi, 2014, 833). To be more specific, it is thought to set the immune system so as not to attack the myelin, so as to reduce its scarring and damage to the CNS. It has been shown to be safe and well-tolerated. Some

As a medical practitioner, I was always fascinated by the complexities of the human nervous system. A few years later, during my neurology residency training, I developed special interests in the field of neurodegenerative disorders and dementias. These are largely non-curable disorders

form of myosin ATP and are not very good at delivering calcium to the muscle