Acquired non-inflammatory myopathy (ANIM) is a neurological disorder that primarily affects the skeletal muscle, most commonly in the limbs of the human body, resulting in muscle weakness or dysfunction. Miopathy refers to problems or abnormalities with myofibrils, which form muscle tissue. In general, non-inflammatory myopathy is a grouping of muscle diseases that is not induced by an autoimmune-mediated inflammatory pathway. These muscle diseases usually arise from a pathology within the muscle tissue itself rather than the nerves that conserve the tissue. ANIM has a wide spectrum of causes that include drugs and toxins, nutritional imbalances, metabolic dysfunction acquired such as defects obtained in protein structure, and infection.
Acquired non-inflammatory myopathy is a different diagnosis of inflammatory myopathy. Inflammatory myopathy is a direct result of some types of autoimmune mediation pathways whereas ANIM is not the result of immune system dysfunction. In addition, the cause of inflammatory myopathy is relatively unknown, whereas many of the causal agents for ANIM have been found that usually affect the structural integrity and function of muscle fibers.
Most myopathies are usually first diagnosed and classified as idiopathic inflammatory myopathy. However, an ANIM diagnosis occurs when the cause of myopathy is found not to arise from the autoimmune mechanism.
Video Acquired non-inflammatory myopathy
Symptoms
Patients with non-inflammatory myopathy acquired typically experience weakness, cramps, stiffness, and tetany, most often in skeletal muscles surrounding the limbs and upper shoulder girdles.
The most frequently reported symptoms are:
- Muscle fatigue
- Pain
- Muscle and cramp spasms
- Tingling
- Numb
- Tetany
- Loss of coordination and balance
- Lack of fine and rough motor control
- Muscle stools and atrophy
Maps Acquired non-inflammatory myopathy
Cause
Acquired non-inflammatory myopathy can be caused by a variety of factors including metabolic abnormalities, medications, nutritional deficiencies, trauma, and upstream abnormalities resulting in decreased function. The two most common causes of ANIM are hyperthyroidism and excessive use of steroids, while many of the drugs used to treat rheumatism are known to be induced agents. Most ANIM cases can be associated with drugs or eating disorders.
Drug induced myopathy
Not infrequently drugs damage muscle fibers. Certain families of drugs are known to induce myopathies at the molecular level, thus altering the function of organelles such as mitochondria. The use of several drugs from these families in relation to each other can increase the risk of developing myopathy. Many of the drugs associated with inducing myopathy in patients are found in rheumatology practice.
Statins
- The statins determined for dyslipidemia are associated with muscle toxicity. Symptoms of muscle toxicity include a combination of cramps, weakness, pain or pain; and often experienced in the quadriceps, chest, biceps, lower back, or abdominal area. Symptoms tend to worsen with muscle exercises, and often continue after the patient is excluded from statin therapy. Common types of myopathy due to statins include myalgia, myositis, and rhabdomyolysis. Statins induce myopathy by inhibiting protein synthesis in the muscle. Statin therapy tends to show no histopathological difference, and thus biopsy does not reveal too much about the damage. Often, damage is found within the mitochondria.
Corticosteroids
- Corticosteroids often cause muscle weakness to some degree in patients. Symptoms are usually weak in the proximal muscle, the flexor of the neck, and in extreme cases, respiratory muscle weakness may also occur. Not only corticosteroids are found to cause some degree of muscle atrophy, but also local or diffuse cell death. These side effects are more common in women than in men, for unknown reasons. EMG prohibits the potential of low amplitude motors, and lack of spontaneous electrical activity.
Colchicine
- Patients who begin taking colchicine, and who have compromised renal function, develop myopathy that exhibits symptoms of proximal muscle weakness, loss of distal sensors and areflexia. Muscle biopsy shows vacuolar myopathy without death or significant cell inflammation.
Chloroquine/Hydroxychloroquine
- Chloroquine/hydroxychloroquine prescription may cause progressive slow progressive muscle weakening that begins in the lower extremities, and moves into the upper limb. Muscle enzyme increases, usually lactate dehydrogenase (LDH).
(HMG-CoA) Reductase Inhibitor
- (HMG-CoA) reductase inhibitors are commonly used in clinics to reduce lipid levels in patients. This drug is known to have toxic effects on myofibrils, resulting in muscle aches and pains. Biopsy shows more damage and molecular dysfunction in the mitochondria, higher lipid storage, and live red myofibrils. These symptoms are usually found in the body's proximal muscles.
Induced Myopathy Diet and Trauma
Many dietary factors and irregularities can cause ANIM. Chemical imbalances caused by abnormal diet can affect muscles directly or cause abnormal function in the upstream path.
- Excess consumption of iodine, especially in the form of seaweed, can cause hyperthyroidism. Hyperthyroidism is one of the most common ways to get ANIM. Hyperactive thyroid gland produces excessive amounts of T3 and T4 hormones that increase metabolism and increase the effects of the sympathetic nervous system. The muscles show a pathology similar to an epinephrine overdose (commonly known as adrenaline). Patients with hyperthyroidism exhibit muscle weakness of the shoulder girdle especially with this condition often asymptomatic. More serious core and leg muscle weakness may occur.
- Vitamin D deficiency in foods is most often associated with osteoporosis, but it can cause ANIM as well. Vitamin D induced ANIM is most commonly associated with sleep deprivation because it induces tonsillar and adenotonsillary hypertrophy, as well as debilitating the airway muscle. This change induces sleep disturbance and sleep disturbance. Vitamin D induced ANM may also be associated with daytime disturbances through this pathway.
Trauma to any muscle is also a common cause for acute ANIM. This is due to muscle contusions and partial or complete loss of function to affected muscle groups.
Diagnosis
The patient's history is one of the key factors in diagnosing the non-inflammatory myopathy obtained. History is used not only to analyze the time frame in which the patient begins to reveal symptoms, but also to see if the disease is present in the patient's family history, to check the history of drug or drug use, and to see if the patient has suffered any trauma due to illness or infection. The basic exam will test where muscle weakness and how weak. This is done by testing the strength of proximal and distal muscles, as well as testing the signs of neurogenic symptoms such as sensation disorders, deep tendon reflexes, and atrophy.
If required, more sophisticated equipment can be used to help determine if a patient has ANIM. These include:
- Measurement of serum levels of muscle enzyme
- Electromyography (EMG)
- Magnetic Resonance Imaging (MRI)
- Muscle biopsy
When examining serum levels of muscle enzymes, the relative levels of creatin kinase, aldolase, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase are carefully examined. Abnormal levels of these proteins show both inflammatory myopathy and ANIM.
EMG is very useful in finding the affected muscle groups, as well as determining the distribution of myopathy throughout the cells. EMG measures several indicators of myopathy such as:
- Spontaneous electrical motion of a single muscle fiber at rest,
- Measurement of polyphase amplitude, shorter amplitudes, motor unit action during muscle stimulation,
- Determine that muscle groups can not distinguish the stimulation of large motor plates from the stimulation of small motor plates involved in recruiting muscle fibers.
Magnetic resonance imaging will cause edema in inflammatory patients, but most likely will not show anything in patients with ANIM and if that happens, it will show some atrophy.
If the individual ANIM is the result of a metabolite defect, additional tests are required. These tests are directed at the function of the enzyme at rest and during exercise, and enzyme intermediates. Molecular genetic testing is often used to determine whether there is a predisposition to the symptoms expressed.
Screening
During strong ischemic exercise, skeletal muscle function is aerobic, producing lactate and ammonia is a coproduct of the myoadenylate deaminase (AMPD) muscle activity. The lower arm ischemic training test takes advantage of this physiology and has been standardized to screen for glycogen metabolism and AMPD deficiency disorders. Patients with glycogen storage disease showed a normal increase in ammonia but no change from baseline lactate, whereas in those with AMPD deficiency, lactate levels increased but ammonia levels did not. If an ischemic exercise test results abnormally, enzyme analysis should be performed on the muscle to confirm the putative deficiency state because false-positive results can occur.
Treatment
Treatment for the non-inflammatory myopathy obtained is directed at the resolution of underlying conditions, pain management, and muscle rehabilitation. ANIM-induced drugs can be reversed or repaired by reducing drugs and seeking alternative treatments. ANIM-induced hyperthyroidism can be treated by anti-thyroid drugs, surgery and not eating high-iodine foods such as seaweed. Treatment of hyperthyroidism results in complete restoration of myopathy. ANIM caused by vitamin D deficiency can be easily solved by taking vitamin supplements and increasing one's exposure to direct sunlight.
Pain can be managed through massaging the affected area and use of nonsteroidal anti-inflammatory drugs (NSAIDs). Exercise, physical therapy, and occupational therapy can be used to rehabilitate affected muscle areas and counteract the atrophy process.
As with all myopathy, the use of walking aids, sticks, and braces can help the mobility of the affected individual.
Direction of research
Diagnostic tests for associated necroterine myopathy associated with associated statins will soon be available to distinguish between different types of myopathy during diagnosis. The presence of spontaneous abnormal electrical activity in the resting muscles indicates an irritable myopathy and is postulated to reflect the existence of a myopathic active necrosis process or unstable muscle membrane potential. However, these findings have poor sensitivity and specificity to predict the presence of inflammatory myopathy in biopsies. Further research on spontaneous electrical activity will allow a more accurate differential diagnosis between various myopathies.
Currently muscle biopsy remains a critical test, unless the diagnosis can be secured by genetic testing. Genetic testing is a less invasive test and if it can be fixed, it would be ideal. Molecular genetic testing is now available for many of the more common metabolic myopathies and muscular dystrophy. These tests are expensive and therefore best used to confirm rather than screening for the diagnosis of specific myopathies. Because of the cost of these tests, these tests are best used to confirm rather than screening for the diagnosis of specific myopathies. It is the researcher's hope that since this testing method improves functionality, cost and access will become more manageable
Increased muscular pathophysiology studies are particularly important for researchers as it helps to better differentiate inflammation rather than non-inflammatory and for medicinal purposes as part of the differential diagnosis. Of course a better classification scheme defining different kinds of myopathy will help doctors to gain a better understanding of how these patients are thinking. Further research efforts to help reward pathophysiology will enhance physicians' ability to manage the most appropriate therapy based on certain variations of myopathy.
The mechanisms for myopathy in individuals with low vitamin D are not fully understood. Decreased availability of 250HD leads to mismanagement of cellular calcium transport to the sarcoplasmic and mitochondrial reticulum, and is associated with reduction of actofybrin myomyosine content.
See also
Inflammatory myopathy
Skeletal striated muscle
Motor unit
References
Source of the article : Wikipedia
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