One of the hallmarks of arterial claudication is that it occurs intermittently. It disappears after a very brief rest and the patient can start walking again until the pain recurs.

The following signs are general signs of atherosclerosis of the lower extremity arteries:

- cyanosis

- atrophic changes like loss of hair, shiny skin

- decreased temperature

- decreased pulse

- redness when limb is returned to a "dependent" position (part of Buerger's test)

All the "P"s

- Pallor increase

- Pulses decreased

- Perishing cold

- Pain

- Paraesthesia

- Paralysis

Intermittent vascular (or arterial) claudication (Latin: "claudicatio intermittens") most often refers to cramping pains in the buttock or leg muscles, especially the calves. It is caused by poor circulation of the blood to the affected area, called Peripheral artery disease. The poor blood flow is often a result of atherosclerotic blockages more proximal to the affected area; individuals with intermittent claudication may have diabetes — often undiagnosed. Another cause, or exacerbating factor, is excessive sitting (several hours), especially in the absence of reasonable breaks, along with a general lack of walking or other exercise that stimulates the legs.

Vascular (or arterial) claudication typically occurs after activity or ambulation for a distance with resultant vascular insufficiency (lack of blood flow) where the muscular demands of oxygen outweighs the supply. Symptoms are lower extremity cramping. Resting from activity even in a standing position may help relieve the symptoms. Spinal or neurogenic claudication may be differentiated from arterial claudication based on activity and position. In neurogenic claudication, positional changes lead to increased stenosis (narrowing) of the spinal canal and compression of nerve roots and resultant lower extremity symptoms. Standing and extension of the spine narrows the spinal canal diameter. Sitting and flexion of the spine increases spinal canal diameter. A person with neurogenic claudication will have worsening of leg cramping with standing erect or standing and walking. Symptoms may be relieved by sitting down (flexing the spine) or even by walking while leaning over (flexion of the spine) a shopping cart.

The ability to ride a stationary bike for a prolonged period of time differentiates neurogenic claudication from vascular claudication. Weakness is also a prominent feature of spinal claudication that is not usually present in intermittent claudication.

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.

Neurogenic claudication (NC), also known as pseudoclaudication, is a common symptom of lumbar spinal stenosis (LSS), causing impingement or inflammation of the nerves emanating from the spinal cord. Neurogenic means that the problem originates with a problem at a nerve, and claudication, from the Latin for limp, because the patient feels a painful cramping or weakness in the legs. NC should therefore be distinguished from vascular claudication, which is when the claudication stems from a circulatory problem, not a neural problem.

Neurogenic claudication may present in one or both legs and usually presents as some combination of discomfort, pain, numbness and weakness in the calves, buttocks, and/or thighs. In some patients, it is precipitated by walking and prolonged standing. The pain is classically relieved by a change in position or flexion of the waist. Although a flexed position may also potentially relieve symptoms, resting typically offers the greatest relief of pain.

Therefore, patients with neurogenic intermittent claudication have less disability in climbing steps, pushing carts and cycling. This is because those movements flex the lumbar spine, and the vertebral foramen widen.

The pathophysiology is thought to be ischemia of the lumbosacral nerve roots secondary to compression from surrounding structures, hypertrophied facets, ligamentum flavum, bone spurs, scar tissue, and bulging or herniated discs.

In addition to vascular claudication, pseudo-trochanteric bursitis should be considered in differential diagnosis.

Up to 50% of people with PAD may have no symptoms. Symptoms of PAD in the legs and feet are generally divided into 2 categories:

1. Intermittent claudication—pain in muscles when walking or using the affected muscles that is relieved by resting those muscles. This is due to the unmet oxygen demand in muscles with use in the setting of inadequate blood flow.

2. Critical limb ischemia, consisting of:

Medical signs of PAD in the legs, due to inadequate perfusion, include:

- Noticeable change in color – blueness, or in temperature (coolness) when compared to the other limb.

- Buerger's test can check for pallor on elevation of limb and redness (rubor) on a change to a sitting position, in an assessment of arterial sufficiency.

- Diminished hair and nail growth on affected limb and digits

PAD in other parts of the body depends on the organ affected. Renal artery stenosis can cause renovascular hypertension.

Carotid artery disease can cause strokes and transient ischemic attacks.

Classically, it is described in male patients as a triad of the following signs and symptoms:

1. claudication of the buttocks and thighs

2. absent or decreased femoral pulses

3. erectile dysfunction

This combination is known as Leriche syndrome. However, any number of symptoms may present, depending on the distribution and severity of the disease, such as muscle atrophy, slow wound healing in the legs, and critical limb ischemia.

Peripheral artery disease (PAD) is a narrowing of the arteries other than those that supply the heart or the brain. When narrowing occurs in the heart, it is called coronary artery disease, while, in the brain, it is called cerebrovascular disease. Peripheral artery disease most commonly affects the legs, but other arteries may also be involved. The classic symptom is leg pain when walking which resolves with rest, known as intermittent claudication. Other symptoms including skin ulcers, bluish skin, cold skin, or poor nail and hair growth may occur in the affected leg. Complications may include an infection or tissue death which may require amputation; coronary artery disease, or stroke. Up to 50% of cases of PAD are without symptoms.

The main risk factor is cigarette smoking. Other risk factors include diabetes, high blood pressure, and high blood cholesterol. The underlying mechanism is usually atherosclerosis. Other causes include artery spasm. PAD is typically diagnosed by finding an ankle-brachial index (ABI) less than 0.90, which is the systolic blood pressure at the ankle divided by the systolic blood pressure of the arm. Duplex ultrasonography and angiography may also be used. Angiography is more accurate and allows for treatment at the same time; however, it is associated with greater risks.

It is unclear if screening for disease is useful as it has not been properly studied. In those with intermittent claudication from PAD, stopping smoking and supervised exercise therapy improves outcomes. Medications, including statins, ACE inhibitors, and cilostazol also may help. Aspirin does not appear to help those with mild disease but is usually recommended in those with more significant disease. Anticoagulants such as warfarin are not typically of benefit. Procedures used to treat the disease include bypass grafting, angioplasty, and atherectomy.

In 2015 about 155 million people had PAD worldwide. In the developed world it affects about 5.3% of 45 to 50 years olds and 18.6% of 85- to 90-year-olds. In the developing world it affects 4.6% of people between the ages of 45 to 50 and 15% of people between the ages of 85 to 90. In the developed world PAD is equally common among men and women while in the developing world women are more commonly affected. In 2015 PAD resulted in about 52,500 deaths up from 16,000 deaths in 1990.

Patients with mesenteric, or intestinal FMD, may experience abdominal pain after eating or weight loss. FMD within the extremities may cause claudication or may be detectable by bruits. If the lower limb arteries are affected, the patient may present with cold legs or evidence of distal embolic disease. FMD present in the subclavian artery may cause arm weakness, parenthesis, claudication, and subclavial steal syndrome.

Jaw claudication is pain in the jaw associated with chewing. It is a classic symptom of Giant-cell arteritis, but can be confused with symptoms of Temporomandibular joint disease, Rheumatoid arthritis of the temporomandibular joint, Myasthenia gravis, tumors of the Parotid gland, or occlusion or stenosis of the External carotid artery. The term is derived by analogy from claudication of the leg, where pain is caused by arterial insufficiency.

There is a recurrent acute and chronic inflammation and thrombosis of arteries and veins of the hands and feet. The main symptom is pain in the affected areas, at rest and while walking (claudication). The impaired circulation increases sensitivity to cold. Peripheral pulses are diminished or absent. There are color changes in the extremities. The colour may range from cyanotic blue to reddish blue. Skin becomes thin and shiny. Hair growth is reduced. Ulcerations and gangrene in the extremities are common complications, often resulting in the need for amputation of the involved extremity.

In medicine, aortoiliac occlusive disease, also known as Leriche's syndrome and Leriche syndrome, is a form of central artery disease involving the blockage of the abdominal aorta as it transitions into the common iliac arteries.

Children with FMD often report various non-specific symptoms or present with hypertension during routine physical examinations. Symptoms are commonly associated with the artery being affected. Symptoms may include headaches, insomnia, fatigue and chest or abdominal pain. FMD affecting the arteries of the head neck are commonly recognized as a cause of childhood strokes.

Detection may stem from a bruit being present over the affected vascular bed during a physical assessment. Yet, absence of a bruit does not rule out significant vascular disease.

In children, renovascular disease accounts for approximately 10% of all causes of secondary hypertension. Kidney failure is a common presentation in infants and children but is uncommon in adults, although it is occasionally the presenting problem in adults with focal disease. “The presentation in infants and children younger than 4 years is especially likely to resemble vacuities.”

Some people develop an initial "inflammatory phase" characterized by systemic illness with signs and symptoms of malaise, fever, night sweats, weight loss, joint pain, fatigue, and fainting. Fainting may result from subclavian steal syndrome or carotid sinus hypersensitivity. There is also often anemia and marked elevation of the ESR or C-reactive protein (nonspecific markers of inflammation). The initial "inflammatory phase" is often followed by a secondary "pulseless phase". The "pulseless phase" is characterized by vascular insufficiency from intimal narrowing of the vessels manifesting as arm or leg claudication, renal artery stenosis causing hypertension, and neurological manifestations due to decreased blood flow to the brain.

Of note is the function of renal artery stenosis in the causation of high blood pressure: Normally perfused kidneys produce a proportionate amount of a substance called renin. Stenosis of the renal arteries causes hypoperfusion (decreased blood flow) of the juxtaglomerular apparatus, resulting in exaggerated secretion of renin, and high blood levels of aldosterone, eventually leading to water and salt retention and high blood pressure. The neurological symptoms of the disease vary depending on the degree; the nature of the blood vessel obstruction; and can range from lightheadedness to seizures (in severe cases). One rare, important feature of the Takayasu's arteritis is ocular involvement in form of visual field defects, vision loss, or retinal hemorrhage. Some individuals with Takayasu's arteritis may present with only late vascular changes, without a preceding systemic illness. In the late stage, weakness of the arterial walls may give rise to localized aneurysms. As with all aneurysms, the possibility of rupture and vascular bleeding is existent and requires monitoring. In view of the chronic process and good collateral development, Raynaud's phenomenon or digital gangrene are very rare in Takayasu arteritis. A rare complication of this condition are coronary artery aneurysms.

Angina pectoris can be quite painful, but many patients with angina complain of chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in the epigastrium (upper central abdomen), back, neck area, jaw, or shoulders. This is explained by the concept of referred pain, and is due to the fact that the spinal level that receives visceral sensation from the heart simultaneously receives cutaneous sensation from parts of the skin specified by that spinal nerve's dermatome, without an ability to discriminate the two. Typical locations for referred pain are arms (often inner left arm), shoulders, and neck into the jaw. Angina is typically precipitated by exertion or emotional stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be accompanied by breathlessness, sweating, and nausea in some cases. In this case, the pulse rate and the blood pressure increases. Chest pain lasting only a few seconds is normally not angina (such as precordial catch syndrome).

Myocardial ischemia comes about when the myocardium (the heart muscle) receives insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardium or because of decreased supply to the myocardium. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients are directly correlated to blocked or narrowed blood vessels.

Some experience "autonomic symptoms" (related to increased activity of the autonomic nervous system) such as nausea, vomiting, and pallor.

Major risk factors for angina include cigarette smoking, diabetes, high cholesterol, high blood pressure, sedentary lifestyle, and family history of premature heart disease.

A variant form of angina—Prinzmetal's angina—occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is believed caused by spasms of the artery. It occurs more in younger women.

Coital angina, also known as "angina d'amour", is angina subsequent to sexual intercourse. It is generally rare, except in patients with severe coronary artery disease.

Also known as 'effort angina', this refers to the classic type of angina related to myocardial ischemia. A typical presentation of stable angina is that of chest discomfort and associated symptoms precipitated by some activity (running, walking, etc.) with minimal or non-existent symptoms at rest or after administration of sublingual nitroglycerin. Symptoms typically abate several minutes after activity and recur when activity resumes. In this way, stable angina may be thought of as being similar to intermittent claudication symptoms. Other recognized precipitants of stable angina include cold weather, heavy meals, and emotional stress.

Takayasu's arteritis (also known as Takayasu's disease, "aortic arch syndrome," "nonspecific aortoarteritis," and "pulseless disease") is a form of large vessel granulomatous vasculitis with massive intimal fibrosis and vascular narrowing, most commonly affecting often young or middle-age women of Asian descent, though anyone can be affected. It mainly affects the aorta (the main blood vessel leaving the heart) and its branches, as well as the pulmonary arteries. Females are about 8–9 times more likely to be affected than males.

Those with the disease often notice symptoms between 15 and 30 years of age. In the Western world, atherosclerosis is a more frequent cause of obstruction of the aortic arch vessels than Takayasu's arteritis. Takayasu's arteritis is similar to other forms of vasculitis, including giant cell arteritis which typically affects older individuals. Due to obstruction of the main branches of the aorta, including the left common carotid artery, the brachiocephalic artery, and the left subclavian artery, Takayasu's arteritis can present as pulseless upper extremities (arms, hands, and wrists with weak or absent pulses on the physical examination) which may be why it is also commonly referred to as the "pulseless disease." Involvement of renal arteries may lead to a presentation of renovascular hypertension.

A concrete diagnosis of thromboangiitis obliterans is often difficult as it relies heavily on exclusion of other conditions. The commonly followed diagnostic criteria are outlined below although the criteria tend to differ slightly from author to author. Olin (2000) proposes the following criteria:

1. Typically between 20–40 years old and male, although recently females have been diagnosed.

2. Current (or recent) history of tobacco use.

3. Presence of distal extremity ischemia (indicated by claudication, pain at rest, ischemic ulcers or gangrene) documented by noninvasive vascular testing such as ultrasound.

4. Exclusion of other autoimmune diseases, hypercoagulable states, and diabetes mellitus by laboratory tests.

5. Exclusion of a proximal source of emboli by echocardiography and arteriography.

6. Consistent arteriographic findings in the clinically involved and noninvolved limbs.

Buerger’s disease can be mimicked by a wide variety of other diseases that cause diminished blood flow to the extremities. These other disorders must be ruled out with an aggressive evaluation, because their treatments differ substantially from that of Buerger’s disease, for which there is no treatment known to be effective.

Diseases with which Buerger’s disease may be confused include atherosclerosis (build-up of cholesterol plaques in the arteries), endocarditis (an infection of the lining of the heart), other types of vasculitis, severe Raynaud's phenomenon associated with connective tissue disorders (e.g., lupus or scleroderma), clotting disorders of the blood, and others.

Angiograms of the upper and lower extremities can be helpful in making the diagnosis of Buerger’s disease. In the proper clinical setting, certain angiographic findings are diagnostic of Buerger’s. These findings include a “corkscrew” appearance of arteries that result from vascular damage, particularly the arteries in the region of the wrists and ankles. Collateral circulation gives "tree root" or "spider leg" appearance. Angiograms may also show occlusions (blockages) or stenosis (narrowings) in multiple areas of both the arms and legs. Distal plethysmography also yields useful information about circulatory status in digits.

To rule out other forms of vasculitis (by excluding involvement of vascular regions atypical for Buerger’s), it is sometimes necessary to perform angiograms of other body regions (e.g., a mesenteric angiogram).

Skin biopsies of affected extremities are rarely performed because of the frequent concern that a biopsy site near an area poorly perfused with blood will not heal well.

Understanding the meaning of signs and symptoms for the clinical syndrome of lumbar stenosis requires an understanding of what the syndrome is, and the prevalence of the condition. A recent review on lumbar stenosis in the Journal of the American Medical Association's "Rational Clinical Examination Series" emphasized that the syndrome can be considered when lower extremity pain occurs in combination with back pain. This syndrome occurs in 12% of older community dwelling men and up to 21% of those in retirement communities.

The leg symptoms in lumbar spinal stenosis (LSS) are similar to those found with vascular claudication, giving rise to the term pseudoclaudication. These symptoms include pain, weakness, and tingling of the legs, which may radiate down the leg to the feet. Additional symptoms in the legs may be fatigue, heaviness, weakness, a sensation of tingling, pricking, or numbness and leg cramps, as well as bladder symptoms. Symptoms are most commonly bilateral and symmetrical, but they may be unilateral; leg pain is usually more troubling than back pain.

Pseudoclaudication, now referred to as neurogenic claudication, typically worsen with standing or walking and improve with sitting. The occurrence is often related to posture and lumbar extension. Lying on the side is often more comfortable than lying flat, since it permits greater lumbar flexion. Vascular claudication can resemble spinal stenosis, and some individuals experience unilateral or bilateral symptoms radiating down the legs rather than true claudication.

The first symptoms of stenosis include bouts of low back pain. After a few months or years, this may progress to claudication. The pain may be radicular, following the classic neurologic pathways. This occurs as the spinal nerves or spinal cord become increasingly trapped in a smaller space within the canal. It can be difficult to determine whether pain in the elderly is caused by lack of blood supply or stenosis; testing can usually differentiate between them but patients can have both vascular disease in the legs and spinal stenosis.

Among people with lower extremity pain in combination with back pain, lumbar stenosis as the cause is two times more likely in those older than 70 years of age while those younger than 60 years it is 0.40 as likely. The character of the pain is also useful. When the discomfort does not occur while seated, the likelihood of LSS increases considerably around 7.4 times. Other features increasing the likelihood of lumbar stenosis are improvement in symptoms on bending forward 6.4 times, pain that occurs in both buttocks or legs 6.3 times, and the presence of neurogenic claudication 3.7 times. Alternately, the absence of neurogenic claudication makes lumbar stenosis much less likely as the explanation for the pain.

Amaurosis fugax (Latin "" meaning "fleeting", Greek "" meaning "darkening", "dark", or "obscure") is a painless temporary loss of vision in one or both eyes.

It is more common in women than in men by a ratio of 2:1 and more common in those of Northern European descent, as well as those residing at higher (northern/southern) latitudes. The mean age of onset is >55 years, and it is rare in those younger than 55 years of age.

People present with:

- bruits

- fever

- headache

- tenderness and sensitivity on the scalp

- jaw claudication (pain in jaw when chewing)

- tongue claudication (pain in tongue when chewing) and necrosis

- reduced visual acuity (blurred vision)

- acute visual loss (sudden blindness)

- diplopia (double vision)

- acute tinnitus (ringing in the ears)

- polymyalgia rheumatica (in 50%)

The inflammation may affect blood supply to the eye; blurred vision or sudden blindness may occur. In 76% of cases involving the eye, the ophthalmic artery is involved causing arteritic anterior ischemic optic neuropathy.

Giant-cell arteritis may present with atypical or overlapping features. Early and accurate diagnosis is important to prevent ischemic vision loss. Therefore, this condition is considered a medical emergency.

Temporal arteritis, the second type of giant cell arteritis, is also a chronic, inflammatory disease involving mid- to large-sized arteries. Temporal arteritis has a higher incidence in people of Scandinavian descent. However, the incidence rate differs based on population, region and races. Temporal arteritis is not uncommon in North America. The incidence rate is around 0.017% for individuals over 50 years of age.

Symptoms of temporal arteritis are classified as specific and nonspecific.

Nonspecific symptoms:

- Headache

- Low grade fever

- Sweating

- Anorexia (loss of appetite)

- Weight loss

- General malaise

Specific symptoms:

- Claudication of the jaw

- Engorged, tender vessels

Specific symptoms usually develop in the advanced stages of temporal arteritis.

Polyarteritis nodosa of unknown mechanism can cause testiscular pain. It is often associated with aneurysms and Hepatitis B.

Spinal stenosis may be congenital (rarely) or acquired (degenerative), overlapping changes normally seen in the aging spine.

The experience of amaurosis fugax is classically described as a temporary loss of vision in one or both eyes that appears as a black "curtain coming down vertically into the field of vision in one eye;" however, this altitudinal visual loss is relatively uncommon. In one study, only 23.8 percent of patients with transient monocular vision loss experienced the classic "curtain" or "shade" descending over their vision. Other descriptions of this experience include a monocular blindness, dimming, fogging, or blurring. Total or sectorial vision loss typically lasts only a few seconds, but may last minutes or even hours. Duration depends on the cause of the vision loss. Obscured vision due to papilledema may last only seconds, while a severely atherosclerotic carotid artery may be associated with a duration of one to ten minutes. Certainly, additional symptoms may be present with the amaurosis fugax, and those findings will depend on the cause of the transient monocular vision loss.

Symptoms of general arteritis may include:

- Inflammation

- Fever

- Increased production of red blood cells (erythrocytes)

- Limping

- Reduced pulse