Imaging is indicated when there are red flags, ongoing neurological symptoms that do not resolve, or ongoing or worsening pain. In particular, early use of imaging (either MRI or CT) is recommended for suspected cancer, infection, or cauda equina syndrome. MRI is slightly better than CT for identifying disc disease; the two technologies are equally useful for diagnosing spinal stenosis. Only a few physical diagnostic tests are helpful. The straight leg raise test is almost always positive in those with disc herniation. Lumbar provocative discography may be useful to identify a specific disc causing pain in those with chronic high levels of low back pain. Similarly, therapeutic procedures such as nerve blocks can be used to determine a specific source of pain. Some evidence supports the use of facet joint injections, transforminal epidural injections and sacroilliac injections as diagnostic tests. Most other physical tests, such as evaluating for scoliosis, muscle weakness or wasting, and impaired reflexes, are of little use.

Complaints of low back pain are one of the most common reasons people visit doctors. For pain that has lasted only a few weeks, the pain is likely to subside on its own. Thus, if a person's medical history and physical examination do not suggest a specific disease as the cause, medical societies advise against imaging tests such as X-rays, CT scans, and MRIs. Individuals may want such tests but, unless red flags are present, they are unnecessary health care. Routine imaging increases costs, is associated with higher rates of surgery with no overall benefit, and the radiation used may be harmful to one's health. Fewer than 1% of imaging tests identify the cause of the problem. Imaging may also detect harmless abnormalities, encouraging people to request further unnecessary testing or to worry. Even so, MRI scans of the lumbar region increased by more than 300% among United States Medicare beneficiaries from 1994 to 2006.

Imaging is not typically needed in the initial diagnosis or treatment of back pain. However, if there are certain "red flag" symptoms present plain radiographs (x-ray), CT scan, or magnetic resonance imaging (MRI) may be recommended. These red flags include:

- History of cancer

- Unexplained weight loss

- Immunosuppression

- Urinary infection

- Intravenous drug use

- Prolonged use of corticosteroids

- Back pain not improved with conservative management

- History of significant trauma

- Minor fall or heavy lift in a potentially osteoporotic or elderly individual

- Acute onset of urinary retention, overflow incontinence, loss of anal sphincter tone, or fecal incontinence

- Saddle anesthesia

- Global or progressive motor weakness in the lower limbs

In most cases of low back pain, medical consensus advises not seeking an exact diagnosis but instead beginning to treat the pain. This assumes that there is no reason to expect that the person has an underlying problem. In most cases, the pain goes away naturally after a few weeks. Typically, people who do seek diagnosis through imaging are not likely to have a better outcome than those who wait for the condition to resolve.

Laboratory testing may include white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).

- Elevated ESR could indicate infection, malignancy, chronic disease, inflammation, trauma, or tissue ischemia.

- Elevated CRP levels are associated with infection.

The presence of certain signs, termed "red flags", indicate the need for further testing to look for more serious underlying problems, which may require immediate or specific treatment. The presence of a red flag does not mean that there is a significant problem. It is only suggestive, and most people with red flags have no serious underlying problem. If no red flags are present, performing diagnostic imaging or laboratory testing in the first four weeks after the start of the symptoms has not been shown to be useful.

The usefulness of many red flags are poorly supported by evidence. The most useful for detecting a fracture are: older age, corticosteroid use, and significant trauma especially if it results in skin markings. The best determinant of the presence of cancer is a history of the same.

With other causes ruled out, people with non-specific low back pain are typically treated symptomatically, without exact determination of the cause. Efforts to uncover factors that might complicate the diagnosis, such as depression, substance abuse, or an agenda concerning insurance payments may be helpful.

Trochleitis is diagnosed based on three criteria: 1) demonstration of inflammation of superior oblique tendon/ trochlea region, 2) periorbital pain and tenderness to palpation in the area of the sore trochlea, and 3) worsening of pain on attempted vertical eye movement, particularly with adduction of the eye. It is important to identify trochleitis because it is a treatable condition and the patient can benefit much from pain relief. Treatment consists of a single injection of corticosteroids to the affected peritrochlear region. A specific "cocktail" consisting of 0.5 ml of depomedrol (80 mg/ml) and 0.5 ml of 2% lidocaine can be injected into the trochlea; immediate relief due to the effects of the local anesthetic indicates successful placement. However, great care must be taken as the injection is in the region of several arteries, veins and nerves. The needle should not be too small (so as not to penetrate tiny structures), the surgeon should draw back on the syringe (to ensure not have pierced a vessel), the lidocaine should not contain epinephrine (which could cause vasospasm), and the pressure of the injection must always be controlled. Only a limited number of injections can be made as they would otherwise lead to muscle atrophy. Diagnosis can be confirmed by response to this treatment; pain and swelling are expected to disappear in 48–72 hours. Some patients experience recurrence of trochleitis.

Weakness or asthenia is a symptom of a number of different conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis.

A diagnostic test for statin-associated auto-immune necrotizing myopathy will be available soon in order to differentiate between different types of myopathies during diagnosis. The presence of abnormal spontaneous electrical activity in the resting muscles indicates an irritable myopathy and is postulated to reflect the presence of an active necrotising myopathic process or unstable muscle membrane potential. However, this finding has poor sensitivity and specificity for predicting the presence of an inflammatory myopathy on biopsy. Further research into this spontaneous electrical activity will allow for a more accurate differential diagnosis between the different myopathies.

Currently a 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 improved upon that would be ideal. Molecular genetic testing is now available for many of the more common metabolic myopathies and muscular dystrophies. These tests are costly and are thus best used to confirm rather than screen for a diagnosis of a specific myopathy. Due to the cost of these tests, they are best used to confirm rather than screen for a diagnosis of a specific myopathy. It is the hope of researchers that as these testing methods improve in function, both costs and access will become more manageable

The increased study of muscle pathophysiology is of importance to researchers as it helps to better differentiate inflammatory versus non-inflammatory and to aim treatment as part of the differential diagnosis. Certainly classification schemes that better define the wide range of myopathies will help clinicians to gain a better understanding of how to think about these patients. Continued research efforts to help appreciate the pathophysiology will improve clinicians ability to administer the most appropriate therapy based on the particular variety of myopathy.

The mechanism for myopathy in individuals with low vitamin D is not completely understood. A decreased availability of 250HD leads to mishandling of cellular calcium transport to the sarcoplasmic reticulum and mitochondria, and is associated with reduced actomyosin content of myofibrils.

A patient's history is one of the key factors in diagnosing acquired noninflammatory myopathy. The history is used not only to analyze the time frame with which the patient began to express symptoms, but to also see if the disease is within the patient's family's history, to check medication or drug use history, and to see if the patient has suffered any trauma due to illness or infection. Basic exams will test for where the muscle weakness is and how weak it is. This is performed by testing for proximal and distal muscle strength, as well as testing for any signs of neurogenic symptoms such as impaired sensation, deep tendon reflexes, and atrophy.

If needed, more advanced equipment can be used to help determine whether a patient is suffering from ANIM. This includes:

- Measurement of serum levels of muscle enzymes

- Electromyography (EMG)

- Magnetic Resonance Imaging (MRI)

- Muscle biopsy

When examining the serum levels of muscle enzymes, the relative levels of creatine kinase, aldolase, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase are closely examined. Abnormal levels of these proteins are indicative of both inflammatory myopathy and ANIM.

EMGs are particularly useful in locating the affected muscle groups, as well as determining the distribution of the myopathy throughout the cell. EMGs measure several indicators of myopathies such as:

- The spontaneous electrical movement from a single muscle fiber at rest,

- Measurement of a polyphasic, shorter amplitude, motor unit action potential during muscle stimulation,

- Determining that the muscle group cannot differentiate large motor plate stimulation from small motor plate stimulation involved in recruitment of muscle fibers.

Magnetic Resonance Imaging will elicit edema in inflammatory patients, but it will most likely show nothing in patients with ANIM and if it does, it will show some atrophy.

If an individual's ANIM is a result of a metabolite defect, then additional tests are required. These tests are directed at enzyme function at rest and during exercise, and enzyme intermediates. Molecular genetic testing is often used to determine if there was any predisposition to the expressed symptoms.

There is no consensus reference standard for the diagnosis of carpal tunnel syndrome. A combination of described symptoms, clinical findings, and electrophysiological testing may be used. CTS work up is the most common referral to the electrodiagnostic lab. Historically, diagnosis has been made with the combination of a thorough history and physical examination in conjunction with the use of electrodiagnostic (EDX) testing for confirmation. Additionally, evolving technology has included the use of ultrasonography in the diagnosis of CTS. However, it is well established that physical exam provocative maneuvers lack both sensitivity and specificity. Furthermore, EDX cannot fully exclude the diagnosis of CTS due to the lack of sensitivity. A Joint report published by the American Association of Neuromuscular and Electrodiagostic Medicine (AANEM), the American Academy of Physical Medicine and Rehabilitation (AAPM&R) and the American Academy of Neurology defines practice parameters, standards and guidelines for EDX studies of CTS based on an extensive critical literature review. This joint review concluded median and sensory nerve conduction studies are valid and reproducible in a clinical laboratory setting and a clinical diagnosis of CTS can be made with a sensitivity greater than 85% and specificity greater than 95%. Given the key role of electrodiagnostic testing in the diagnosis of CTS, The American Association of Neuromuscular & Electrodiagnostic Medicine has issued evidence-based practice guidelines, both for the diagnosis of carpal tunnel syndrome.

Numbness in the distribution of the median nerve, nocturnal symptoms, thenar muscle weakness/atrophy, positive Tinel's sign at the carpal tunnel, and abnormal sensory testing such as two-point discrimination have been standardized as clinical diagnostic criteria by consensus panels of experts. Pain may also be a presenting symptom, although less common than sensory disturbances.

Electrodiagnostic testing (electromyography and nerve conduction velocity) can objectively verify the median nerve dysfunction. Normal nerve conduction studies, however, do not exclude the diagnosis of CTS. Clinical assessment by history taking and physical examination can support a diagnosis of CTS. If clinical suspicion of CTS is high, treatment should be initiated despite normal electrodiagnostic testing.

In some conditions, such as myasthenia gravis, muscle strength is normal when resting, but "true weakness" occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions.

Initial screening for CIP/CIM may be performed using an objective scoring system for muscle strength. The Medical Research Council (MRC) score is one such tool, and sometimes used to help identify CIP/CIM patients in research studies. The MRC score involves assessing strength in 3 muscle groups in the right and left sides of both the upper and lower extremities. Each muscle tested is given a score of 0-5, giving a total possible score of 60. An MRC score less than 48 is suggestive of CIP/CIM. However, the tool requires that patients be awake and cooperative, which is often not the case. Also, the screening tool is non-specific, because it does not identify the cause a person's muscle weakness.

Once weakness is detected, the evaluation of muscle strength should be repeated several times. If the weakness persists, then a muscle biopsy, a nerve conduction study (electrophysiological studies), or both should be performed.

Muscle weakness or myasthenia (my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness") is a lack of muscle strength. The causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Muscle weakness can also be caused by low levels of potassium and other electrolytes within muscle cells. It can be temporary or long-lasting (from seconds or minutes to months or years).

There are few disorders on the differential diagnosis for carpal tunnel syndrome. Cervical radiculopathy can be mistaken for carpal tunnel syndrome since it can also cause abnormal or painful sensations in the hands and wrist. In contrast to carpal tunnel syndrome, the symptoms of cervical radiculopathy usually begins in the neck and travels down the affected arm and may be worsened by neck movement. Electromyography and imaging of the cervical spine can help to differentiate cervical radiculopathy from carpal tunnel syndrome if the diagnosis is unclear. Carpal tunnel syndrome is sometimes applied as a label to anyone with pain, numbness, swelling, and/or burning in the radial side of the hands and/or wrists. When pain is the primary symptom, carpal tunnel syndrome is unlikely to be the source of the symptoms. As a whole, the medical community is not currently embracing or accepting trigger point theories due to lack of scientific evidence supporting their effectiveness.

The serum creatine phosphokinase (CPK) can be mildly elevated. While the CPK is often a good marker for damage to muscle tissue, it is not a helpful marker in CIP/CIM, because CIP/CIM is a gradual process and does not usually involve significant muscle cell death (necrosis). Also, even if necrosis is present, it may be brief and is therefore easily missed. If a lumbar puncture (spinal tap) is performed, the protein level in the cerebral spinal fluid would be normal.

Diagnosis can be achieved through a specialized form of electromyographic (EMG) testing called the long exercise test. This test measures the amplitude of a nerve response (called the Compound Muscle Action Potential or CMAP) for 40 to 50 minutes following a few minutes of exercise. In affected patients, there is a progressive fall in the amplitude of the potential. Besides the patient history or a report of serum potassium low normal or low during an attack, the long exercise test is the current standard for medical testing. Genetic diagnosis is often unreliable as only a few of the more common gene locations are tested, but even with more extensive testing 20–37% of people with a clinical diagnosis of hypokalemic periodic paralysis have no known mutation in the two known genes. Standard EMG testing cannot diagnose a patient unless they are in a full blown attack at the time of testing. Provoking an attack with exercise and diet then trying oral potassium can be diagnostic, but also dangerous as this form of PP has an alternate form known as hyperkalemic periodic paralysis. The symptoms are almost the same, but the treatment is different. The old glucose insulin challenge is dangerous and risky to the point of being life-threatening and should never be done when other options are so readily available.

People with hypokalemic periodic paralysis are often misdiagnosed as having a conversion disorder or hysterical paralysis since the weakness is muscle-based and doesn't correspond to nerve or spinal root distributions. The tendency of people with hypokalemic periodic paralysis to get paralyzed when epinephrine is released in "fight or flight" situations further adds to the temptation to misdiagnose the disorder as psychiatric.

Muscle weakness can be classified as either "true" or "perceived" based on its cause.

- True muscle weakness (or neuromuscular weakness) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy.

- Perceived muscle weakness (or non-neuromuscular weakness) describes a condition where a person feels more effort than normal is required to exert a given amount of force but actual muscle strength is normal, for example chronic fatigue syndrome.

In some conditions, such as myasthenia gravis, muscle strength is normal when resting, but "true" weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions.

Testing for gonorrhea and chlamydia should be routinely performed.

Macrophagic Myofasciitis, or MMF, is a rare muscle disease identified in 1993. The disease is characterized by microscopic lesions found in muscle biopsies that show infiltration of muscle tissue by PAS-positive macrophages.

Specific causes of MMF are unknown. Intramuscular injections of aluminium-containing vaccines have been implicated. Many of those affected with the disease had previously been treated for malaria with chloroquine or hydroxychloroquine.

Clinical symptoms include muscle pain, joint pain, muscle weakness, fatigue, fever, and muscle tenderness. A diagnosis can only be identified with an open muscle biopsy of the vaccinated muscle.

Studies at the University of Paris have shown that MMF lesions result when the aluminum hydroxide adjuvant from a vaccine remains embedded in the tissue and causes a steady immune reaction.

As of 2009 and with few exceptions, MMF had only been observed in France.

The cause of trochleitis is often unknown (idiopathic trochleitis), but it has been known to occur in patients with rheumatological diseases such as systemic lupus erythematosus, rheumatoid arthritis, enteropathic arthropathy, and psoriasis. In his study, Tychsen and his group evaluated trochleitis patients with echography and CT scan to demonstrate swelling and inflammation. Imaging studies showed inflammation of superior oblique tendon/ trochlear pulley. It was unclear whether the inflammation involved the trochlea itself, or the tissues surrounding the trochlea.

Intermittent claudication is a symptom and is by definition diagnosed by a patient reporting a history of leg pain with walking relieved by rest. However, as other conditions such as sciatica can mimic intermittent claudication, testing is often performed to confirm the diagnosis of peripheral artery disease.

Magnetic resonance angiography and duplex ultrasonography appear to be slightly more cost-effective in diagnosing peripheral artery disease among people with intermittent claudication than projectional angiography.

Ultrasonography uses sound waves to create an image. It may show where fluid is located in the chest. It also can show some tumors. Although ultrasound may detect fluid around the lungs, also known as a pleural effusion, sound waves are scattered by air. Therefore, an actual picture of the lungs cannot be obtained with ultrasonography.

A CT scan provides a computer-generated picture of the lungs that can show pockets of fluid. It also may show signs of pneumonia, a lung abscess, or a tumor.

Odynophagia may have environmental or behavioral causes, such as:

- Very hot or cold food and drinks

- Taking certain medications

- Using drugs, tobacco, or alcohol

- Trauma or injury to the mouth, throat, or tongue

Compartment syndrome is a clinical diagnosis, i.e., no diagnostic test conclusively proves its presence or absence, but direct measurement of the pressure in a fascial compartment, and the difference between this pressure and the blood pressure, may be used to assess its severity. High pressures in the compartment and a small difference between compartment pressure and blood pressure indicate that the blood supply is likely to be insufficient, and that surgical intervention may be needed.

Disseminated intravascular coagulation, another complication of rhabdomyolysis and other forms of critical illness, may be suspected on the basis of unexpected bleeding or abnormalities in hematological tests, such as a decreasing platelet count or prolongation of the prothrombin time. The diagnosis can be confirmed with standard blood tests for DIC, such as D-dimer.

Proximal muscle weakness, characteristic skin rash and elevated muscle enzymes are routinely used to identify JDM. Typical magnetic resonance imaging and muscle biopsy changes are considered the next most useful diagnostic criteria, followed by myopathic changes on electromyogram, calcinosis, dysphonia and nailfold capillaroscopy. Other useful criteria include myositis-specific or -related antibodies, nailfold capillaroscopy, factor VIII-related antigen, muscle ultrasound, calcinosis and neopterin.