No specific test exists to diagnose polymyalgia rheumatica; many other diseases can cause inflammation and pain in muscles, but a few tests can help narrow down the cause of the pain. Limitation in shoulder motion, or swelling of the joints in the wrists or hands, are noted by the doctor. A patient's answers to questions, a general physical exam, and the results of tests can help a doctor determine the cause of pain and stiffness.

One blood test usually performed is the erythrocyte sedimentation rate (ESR) which measures how fast the patient's red blood cells settle in a test tube. The faster the blood cells settle, the higher the ESR value, which means inflammation is present. Many conditions can cause an elevated ESR, so this test alone is not proof that a person has polymyalgia rheumatica.

Another test that checks the level of C-reactive protein (CRP) in the blood may also be conducted. CRP is produced by the liver in response to an injury or infection, and people with polymyalgia rheumatica usually have high levels. However, like the ESR, this test is also not very specific.

Polymyalgia rheumatica is sometimes associated with temporal arteritis, a condition requiring more aggressive therapy. To test for this additional disorder, a biopsy sample may be taken from the temporal artery.

No circumstances are certain as to which an individual will get polymyalgia rheumatica, but a few factors show a relationship with the disorder.

- Usually, PMR only affects adults over the age of 50.

- The average age of a person who has PMR is about 70 years old.

- Women are twice as likely to get PMR as men.

- Caucasians are more likely to get this disease. It is more likely to affect people of Northern European origin; Scandinavians are especially vulnerable.

- About 50% of people with temporal arteritis also have polymyalgia rheumatica.

Radiological examination of the temporal artery with ultrasound yields a halo sign.

Contrast-enhanced brain MRI and CT is generally negative in this disorder.

Recent studies have shown that 3T MRI using super high resolution imaging and contrast injection can non-invasively diagnose this disorder with high specificity and sensitivity.

The gold standard for diagnosing temporal arteritis is biopsy, which involves removing a small part of the vessel under local anesthesia and examining it microscopically for giant cells infiltrating the tissue. Since the blood vessels are involved in a patchy pattern, there may be unaffected areas on the vessel and the biopsy might have been taken from these parts. Unilateral biopsy of a 1.5–3 cm length is 85-90% sensitive (1 cm is the minimum). A negative result does not definitively rule out the diagnosis. Characterised as intimal hyperplasia and medial granulomatous inflammation with elastic lamina fragmentation with a CD 4+ predominant T cell infiltrate, currently biopsy is only considered confirmatory for the clinical diagnosis, or one of the diagnostic criteria.

Ultrasonography and magnetic resonance imaging of the hands and/or feet have been proposed as useful diagnostic investigations in RS3PE.

Some studies linked RS3PE to HLA-B27 whereas others have not.

RS3PE responds excellently to low dose corticosteroids, with sustained and often complete remission. Non-steroidal anti-inflammatory drugs (NSAIDs) have also been used. Hydroxychloroquine has proven effective in some cases.

Treatment of aortitis depends on the underlying cause. Infectious causes commonly require antibiotic treatment, while those associated with autoimmune vasculitides are generally treated with steroids.

Management includes the following treatment priorities: stop the inflammation, treat complications, prevent and monitor for re-occurrence.

In this table: ANA = Antinuclear antibodies, CRP = C-reactive protein, ESR = Erythrocyte Sedimentation Rate, "ds"DNA = double-stranded DNA, ENA = extractable nuclear antigens, RNP = ribonucleoproteins; VDRL = Venereal Disease Research Laboratory

If untreated, has three distinct phases. The first is a prepulseless inflammatory stage with nonspecific symptoms such as fatigue, arthralgias, and low-grade fevers. Phase two includes vascular inflammation with pain secondary to the condition, along with tenderness to palpation over the site. The last phase includes symptoms of ischemia and pain associated with the use of limbs. Limbs are also cool and clammy in this stage.

Treatments are generally directed toward stopping the inflammation and suppressing the immune system. Typically, corticosteroids such as prednisone are used. Additionally, other immune suppression drugs, such as cyclophosphamide and others, are considered. In case of an infection, antimicrobial agents including cephalexin may be prescribed. Affected organs (such as the heart or lungs) may require specific medical treatment intended to improve their function during the active phase of the disease.

All people who present with red flags indicating a dangerous secondary headache should receive neuroimaging. The best form of neuroimaging for these headaches is controversial. Non-contrast computerized tomography (CT) scan is usually the first step in head imaging as it is readily available in Emergency Departments and hospitals and is cheaper than MRI. Non-contrast CT is best for identifying an acute head bleed. Magnetic Resonance Imaging (MRI) is best for brain tumors and problems in the posterior fossa, or back of the brain. MRI is more sensitive for identifying intracranial problems, however it can pick up brain abnormalities that are not relevant to the person's headaches.

The American College of Radiology recommends the following imaging tests for different specific situations:

A lumbar puncture is a procedure in which cerebral spinal fluid is removed from the spine with a needle. A lumbar puncture is necessary to look for infection or blood in the spinal fluid. A lumbar puncture can also evaluate the pressure in the spinal column, which can be useful for people with idiopathic intracranial hypertension (usually young, obese women who have increased intracranial pressure), or other causes of increased intracranial pressure. In most cases, a CT scan should be done first.

Multiple standards exist for defining Henoch–Schönlein purpura, including the 1990 American College of Rheumatology (ACR) classification and the 1994 Chapel Hill Consensus Conference (CHCC). Some have reported the ACR criteria to be more sensitive than those of the CHCC.

More recent classifications, the 2006 European League Against Rheumatism (EULAR) and Pediatric Rheumatology Society (PReS) classification, include palpable purpura as a mandatory criterion, together with at least one of the following findings: diffuse abdominal pain, predominant IgA deposition (confirmed on skin biopsy), acute arthritis in any joint, and renal involvement (as evidenced by the presence of blood and/or protein in the urine).

Henoch–Schönlein purpura may present with an atypical manifestation, which can be confused with papular urticaria, systemic lupus erythematosus, meningococcemia, dermatitis herpetiformis, and acute hemorrhagic edema of infancy.

Prompt diagnosis is critical, since the sudden blindness in the one eye is often followed, within days, by similar sudden blindness in the second eye. Treatment may prevent further damage (see below). Any patient diagnosed with non-arteritic AION over the age of 50 must be asked about the constitutional symptoms mentioned above. Furthermore, AION patients over the age of 75 should often be blood tested regardless.

There are no characteristic laboratory abnormalities to diagnose CFS; testing is used to rule out other conditions which could be responsible for the symptoms. When symptoms are attributable to certain other conditions, the diagnosis of CFS is excluded. As such, a diagnosis of CFS/ME is generally one of exclusion (of alternative diagnoses).

Certain medical conditions can cause chronic fatigue and must be ruled out before a diagnosis of CFS can be given. Hypothyroidism, anemia, coeliac disease (that can occur without gastrointestinal symptoms), diabetes and certain psychiatric disorders are a few of the diseases that must be ruled out if the patient presents with appropriate symptoms. Other diseases, listed by the Centers for Disease Control and Prevention, include infectious diseases (such as Epstein–Barr virus, influenza, HIV infection, tuberculosis, Lyme disease), neuroendocrine diseases (such as thyroiditis, Addison's disease, adrenal insufficiency, Cushing's disease), hematologic diseases (such as occult malignancy, lymphoma), rheumatologic diseases (such as fibromyalgia, polymyalgia rheumatica, Sjögren's syndrome, giant-cell arteritis, polymyositis, dermatomyositis), psychiatric diseases (such as bipolar disorder, schizophrenia, delusional disorders, dementia, anorexia/bulimia nervosa), neuropsychologic diseases (such as obstructive sleep apnea, parkinsonism, multiple sclerosis), and others (such as nasal obstruction from allergies, sinusitis, anatomic obstruction, autoimmune diseases, some chronic illness, alcohol or substance abuse, pharmacologic side effects, heavy metal exposure and toxicity, marked body weight fluctuation).

Persons with fibromyalgia (FM, or fibromyalgia syndrome, FMS), like those with CFS, have muscle pain, severe fatigue and sleep disturbances. The presence of allodynia (abnormal pain responses to mild stimulation) and of extensive tender points in specific locations differentiates FM from CFS, although the two diseases often co-occur.

Depressive symptoms, if seen in CFS, may be differentially diagnosed from primary depression by the absence of anhedonia, decreased motivation, and guilt; and the presence of somatic symptoms such as sore throat, swollen lymph nodes, and exercise intolerance with post exertional exacerbation of symptoms.

There are several constitutional symptoms of temporal arteritis that may aid in diagnosis of AAION such as jaw claudication (spasms of the jaw muscle), scalp tenderness, unintentional weight loss, fatigue, myalgias and loss of appetite. However, many cases are asymptomatic. There are also elevations in three blood tests that help identify AAION: erythrocyte sedimentation rate (ESR), C reactive protein (CRP) and platelet count (thrombocytosis). A related rheumatic disease called polymyalgia rheumatica has a 15 percent incidence of giant cell arteritis.

Diagnostic procedures that may reveal muscular disorders include direct clinical observations. This usually starts with the observation of bulk, possible atrophy or loss of muscle tone. Neuromuscular disease can also be diagnosed by testing the levels of various chemicals and antigens in the blood, and using electrodiagnostic medicine tests including electromyography (measuring electrical activity in muscles) and nerve conduction studies.

In neuromuscular disease evaluation, it is important to perform musculoskeletal and neurologic examinations. Genetic testing is an important part of diagnosing inherited neuromuscular conditions.

In terms of treatment for neuromuscular diseases (NMD), "exercise" might be a way of managing them, as NMD individuals would gain muscle strength. In a study aimed at results of exercise, in muscular dystrophy and Charcot-Marie-Tooth disease, the later benefited while the former did not show benefit; therefore, it depends on the disease Other management routes for NMD should be based on medicinal and surgical procedures, again depending on the underlying cause.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Aside from discontinuation of glucocorticoid medication, potential treatments discussed in the research literature include:

- anti-glucocorticoids

- psychoactive drugs that up-regulate the GRII glucocorticoid receptor:

- tricyclic antidepressants: Desipramine, Imipramine, and Amitriptyline (SSRIs do not )

- serotonin antagonists: Ketanserin

- mood stabilizers: Lithium

- corticotropin-releasing hormone (CRH) antagonists

- glutamate antagonists

- dehydroepiandrosterone (DHEA)

- small molecule brain-derived neurotrophic factor (BDNF) analogs

- stress reduction therapies and exercise.

Glucocorticoid medications have been known to be associated with significant side effects involving behavior and mood, regardless of previous psychiatric or cognitive condition, since the early 1950s. But cognitive side effects of steroid medications involving memory and attention are not as widely publicized and may be misdiagnosed as separate conditions, such as attention deficit disorder (ADHD or ADD) in children or early Alzheimer's disease in elderly patients.

Vascular-related cutaneous conditions result from dysfunction of the blood or blood vessels in the dermis, or lymphatics in the subcutaneous tissues.

- Aagenaes syndrome

- Acroangiodermatitis (acroangiodermatitis of Mali, Mali acroangiodermatitis, Pseudo-Kaposi's sarcoma)

- Acute hemorrhagic edema of infancy (acute hemorrhagic edema of childhood, Finkelstein's disease, infantile postinfectious iris-like purpura and edema, medallion-like purpura, purpura en cocarde avec oedema, Seidlmayer syndrome)

- Arterial insufficiency ulcer (ischemic ulcer)

- Arteriosclerosis obliterans

- Bier spots

- Blueberry muffin baby

- Bonnet–Dechaume–Blanc syndrome (Wyburn–Mason syndrome)

- Bullous lymphedema

- Bullous small vessel vasculitis (bullous variant of small vessel vasculitis)

- Calciphylaxis

- Caput succedaneum

- Cholesterol embolus (warfarin blue toe syndrome)

- Cobb syndrome

- Corona phlebectatica

- Cryofibrinogenemic purpura

- Cryoglobulinemic purpura

- Cryoglobulinemic vasculitis

- Cutaneous small-vessel vasculitis (cutaneous leukocytoclastic angiitis, cutaneous leukocytoclastic vasculitis, cutaneous necrotizing venulitis, hypersensitivity angiitis)

- Deep venous thrombosis

- Disseminated intravascular coagulation

- Doucas and Kapetanakis pigmented purpura

- Drug-induced purpura

- Drug-induced thrombocytopenic purpura

- Eczematid-like purpura of Doucas and Kapetanakis

- Epidemic dropsy

- Erythema elevatum diutinum

- Erythromelalgia (acromelalgia, erythermalgia)

- Factitial lymphedema (hysterical edema)

- Fibrinolysis syndrome (defibrinating syndrome, hypofibrinogenemia)

- Food-induced purpura

- Generalized essential telangiectasia (general essential telangiectasia)

- Giant-cell arteritis

- Gougerot–Blum syndrome (pigmented purpuric lichenoid dermatitis, pigmented purpuric lichenoid dermatitis of Gougerot and Blum)

- Harlequin color change

- Hematopoietic ulcer

- Hennekam syndrome (Hennekam lymphangiectasia-lymphedema syndrome, intestinal lymphagiectasia-lymphedema-mental retardation syndrome)

- Henoch–Schönlein purpura (anaphylactoid purpura, purpura rheumatica, Schönlein–Henoch purpura)

- Hereditary hemorrhagic telangiectasia (Osler's disease, Osler–Weber–Rendu disease)

- Idiopathic thrombocytopenic purpura (autoimmune thrombocytopenic purpura, Werlhof's disease)

- IgA vasculitis

- Kawasaki's disease (mucocutaneous lymph node syndrome)

- Levamisole-induced vasculitis

- Lichen aureus (lichen purpuricus)

- Livedo racemosa

- Livedo reticularis

- Livedoid dermatitis (embolia cutis medicamentosa, Nicolau syndrome)

- Livedoid vasculopathy (atrophie blanche, livedo reticularis with summer ulceration, livedoid vasculitis, PURPLE syndrome, segmental hyalinizing vasculitis)

- Lymphedema praecox

- Lymphedema–distichiasis syndrome

- Maffucci syndrome

- Majocchi's disease (purpura annularis telangiectodes, purpura annularis telangiectodes of Majocchi)

- Malignant atrophic papulosis (Degos' disease)

- Marshall–White syndrome

- Meige lymphedema

- Microscopic polyangiitis (microscopic polyarteritis, microscopic polyarteritis nodosa)

- Mondor's disease (Mondor's syndrome of superficial thrombophlebitis)

- Neuropathic ulcer (mal perforans)

- Njolstad syndrome

- Nonne–Milroy–Meige syndrome (hereditary lymphedema, Milroy disease)

- Obstructive purpura

- Orthostatic purpura (stasis purpura)

- Painful bruising syndrome (autoerythrocyte sensitization, Gardner–Diamond syndrome, psychogenic purpura)

- Parkes Weber syndrome

- Paroxysmal hand hematoma (Achenbach syndrome)

- Paroxysmal nocturnal hemoglobinuria

- Polyarteritis nodosa (panarteritis nodosa, periarteritis nodosa)

- Postcardiotomy syndrome

- Perinatal gangrene of the buttock

- Pigmentary purpuric eruptions (progressive pigmentary dermatosis, progressive pigmenting purpura, purpura pigmentosa chronica)

- Postinflammatory lymphedema

- Postmastectomy lymphangiosarcoma (Stewart–Treves syndrome)

- Purpura fulminans (purpura gangrenosa)

- Purpura secondary to clotting disorders

- Purpuric agave dermatitis

- Raynaud phenomenon

- Raynaud's disease (primary Raynaud's phenomenon)

- Reactive angioendotheliomatosis

- Schamberg's disease (progressive pigmentary dermatosis of Schamberg, purpura pigmentosa progressiva, Schamberg's purpura)

- Secondary lymphedema

- Septic thrombophlebitis

- Sinusoidal hemangioma

- Sneddon's syndrome (idiopathic livedo reticularis with cerebrovascular accidents)

- Solar purpura (actinic purpura, senile purpura)

- Stasis dermatitis (congestion eczema, gravitational dermatitis, gravitational eczema, stasis eczema, varicose eczema)

- Superficial thrombophlebitis

- Takayasu arteritis (aortic arch syndrome, pulseless disease)

- Temporal arteritis (cranial arteritis, Horton's disease)

- Thromboangiitis obliterans (Buerger's disease)

- Thrombotic thrombocytopenic purpura (Moschcowitz syndrome)

- Traumatic purpura

- Trousseau's syndrome

- Unilateral nevoid telangiectasia (nevoid telangiectasia)

- Urticarial vasculitis (chronic urticaria as a manifestation of venulitis, hypocomplementemic urticarial vasculitis syndrome, hypocomplementemic vasculitis, unusual lupus-like syndrome)

- Venous insufficiency ulceration

- Waldenström hyperglobulinemic purpura (purpura hyperglobulinemica)

- Waldenström macroglobulinemia

- Wegener granulomatosis

- Yellow nail syndrome (primary lymphedema associated with yellow nails and pleural effusion)