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 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.

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.

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 claudication (Latin: "claudicatio intermittens") is a symptom that describes muscle pain on mild exertion (ache, cramp, numbness or sense of fatigue), classically in the calf muscle, which occurs during exercise, such as walking, and is relieved by a short period of rest. It is classically associated with early-stage peripheral artery disease, and can progress to critical limb ischemia unless treated or risk factors are modified.

Claudication derives from the Latin verb "claudicare", "to limp".

TOS affects mainly the upper limbs, with signs and symptoms manifesting in the shoulders, neck, arms and hands. Pain can be present on an intermittent or permanent basis. It can be sharp/stabbing, burning, or aching. TOS can involve only part of the hand (as in the pinky and adjacent half of the ring finger), all of the hand, or the inner aspect of the forearm and upper arm. Pain can also be in the side of the neck, the pectoral area below the clavicle, the armpit/axillary area, and the upper back (i.e., the trapezius and rhomboid area). Discoloration of the hands, one hand colder than the other hand, weakness of the hand and arm muscles, and tingling are commonly present.

TOS is often the underlying cause of refractory upper limb conditions like frozen shoulder and carpal tunnel syndrome that frequently defy standard treatment protocols. TOS can be related to Forward head posture.

A painful, swollen and blue arm, particularly when occurring after strenuous physical activity, could be the first sign of a subclavian vein compression related with an unknown TOS and complicated by thrombosis (blood clots), the so-called Paget–Schroetter syndrome or effort-induced thrombosis.

TOS can be related to cerebrovascular arterial insufficiency when affecting the subclavian artery. It also can affect the vertebral artery, in which case it could produce vision disturbances, including transient blindness, and embolic cerebral infarction.

TOS can also lead to eye problems and vision loss as a circumstance of vertebral artery compression. Although very rare, if compression of the brain stem is also involved in an individual presentation of TOS, transient blindness may occur while the head is held in certain positions.

If left untreated, TOS can lead to neurological deficits as a result of the hypoperfusion and hypometabolism of certain areas of the brain and cerebellum.

Thoracic outlet syndrome (TOS) is a condition in which there is compression of the nerves, arteries, or veins in the passageway from the lower neck to the armpit. There are three main types: neurogenic, venous, and arterial. The neurogenic type is the most common and presents with pain, weakness, and occasionally loss of muscle at the base of the thumb. The venous type results in swelling, pain, and possibly a bluish coloration of the arm. The arterial type results in pain, coldness, and paleness of the arm.

TOS may result from trauma, repetitive arm movements, tumors, pregnancy, or anatomical variations such as a cervical rib. The diagnosis may be supported by nerve conduction studies and medical imaging. Other conditions that can produce similar symptoms include rotator cuff tear, cervical disc disorders, fibromyalgia, multiple sclerosis, and complex regional pain syndrome.

Initial treatment for the neurogenic type is with exercises to strengthen the chest muscles and improve posture. NSAIDs such as naproxen may be used for pain. Surgery is typically done for the arterial and venous types and for the neurogenic type if it does not improve with other treatments. Blood thinners may be used to treat or prevent blood clots. The condition affects about 1% of the population. It is more common in women than men and it occurs most commonly between 20 and 50 years of age. The condition was first described in 1818 and the current term "thoracic outlet syndrome" first used in 1956.

Radiculopathy, also commonly referred to as pinched nerve, refers to a set of conditions in which one or more nerves are affected and do not work properly (a neuropathy). This can result in pain (radicular pain), weakness, numbness, or difficulty controlling specific muscles.

In a radiculopathy, the problem occurs at or near the root of the nerve, shortly after its exit from the spinal cord. However, the pain or other symptoms often radiate to the part of the body served by that nerve. For example, a nerve root impingement in the neck can produce pain and weakness in the forearm. Likewise, an impingement in the lower back or lumbar-sacral spine can be manifested with symptoms in the foot.

The radicular pain that results from a radiculopathy should not be confused with referred pain, which is different both in mechanism and clinical features.

"Polyradiculopathy" refers to the condition where more than one spinal nerve root is affected.

Spinal shock was first defined by Whytt in 1750 as a loss of accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening

In spinal cord injuries above T6, neurogenic shock may occur, from the loss of autonomic innervation from the brain. Parasympathetic is preserved but the synergy between sympathetic and parasympathetic system is lost in cervical and high thoracic SCI lesions. Sacral parasympathetic loss may be encountered in lesions below T6 or T7. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrhythmias – which resolve in 3–6 weeks. Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It is characterized by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder or bowel control, sweating, headaches, and other sympathetic effects.

Radiculopathy is a mechanical compression of a nerve root usually at the exit foramen or lateral recess. It may be secondary to degenerative disc disease, osteoarthritis, facet joint degeneration/hypertrophy, ligamentous hypertrophy, spondylolisthesis, or a combination of these factors. Rarer causes of radiculopathy may include radiation, diabetes mellitus, neoplastic disease, or any meningeal-based disease process. Second-stage Lyme meningitis resembles aseptic meningitis and is often associated with radiculopathies.

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.

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.

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.

Electroanalgesia is a form of analgesia, or pain relief, that uses electricity to ease pain. Electrical devices can be internal or external, at the site of pain (local) or delocalized throughout the whole body. It works by interfering with the electric currents of pain signals, inhibiting them from reaching the brain and inducing a response; different from traditional analgesics, such as opiates which mimic natural endorphins and NSAIDS (non-steroidal anti-inflammatory drugs) that help relieve inflammation and stop pain at the source. Electroanalgesia has a lower addictive potential and poses less health threats to the general public, but can cause serious health problems, even death, in people with other electrical devices such as pacemakers or internal hearing aids, or with heart problems.

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

Neurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder, is a of the urinary bladder due to disease of the central nervous system or peripheral nerves involved in the control of micturition (urination). Neurogenic bladder usually causes difficulty or full inability to pass urine without use of a catheter or other method.

Any condition that impairs bladder and bladder outlet afferent and efferent signaling can cause neurogenic bladder.

It is often associated with spinal cord diseases (such as syringomyelia/hydromyelia), injuries (like herniated disks), and neural tube defects including spina bifida.

It may also be caused by brain tumors and other diseases of the brain, pregnancy and by peripheral nerve diseases such as: Diabetes, Alcoholism (and Vitamin B12 deficiency).

It is a common complication of major surgery in the pelvis, such as for removal of sacrococcygeal teratoma and other tumors.

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.

Neurogenic shock is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system such as spinal cord injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting in pooling of blood within the extremities lacking sympathetic tone. The slowed heart rate results from unopposed vagal activity and has been found to be exacerbated by hypoxia and endobronchial suction.

Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated. It is not to be confused with spinal shock, which is not circulatory in nature.

The pathophysiology of the condition results from neuronal plasticity associated with bladder afferents and motor neurons innervating the external urethral sphincter. People with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition.

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.

Because it causes a loss of sympathetic tone, which plays a major role in other forms of shock, neurogenic shock causes a unique and atypical presentation.

Typically, in other forms of shock, the sympathetic nervous system triggers various compensatory mechanisms by releasing epinephrine and norepinephrine, its major chemical mediators. These neurotransmitters trigger an increased heart rate, faster breathing, and sweating. They also trigger vasoconstriction, to shunt blood away from the extremities and to the vital organs.

In neurogenic shock, the body loses its ability to activate the sympathetic nervous system and cannot trigger these compensatory mechanisms. Only parasympathetic tone remains. Consequently, neurogenic shock's unique presentation includes:

- Instantaneous hypotension due to sudden, massive vasodilation

- Warm, flushed skin due to vasodilation and inability to vasoconstrict

- Priapism, also due to vasodilation

- The patient will be unable to get tachycardic, and may become bradycardic

- If the injury is below the 5th cervical vertebra, the patient will exhibit diaphragmatic breathing due to loss of nervous control of the intercostal muscles (which are required for thoracic breathing).

- If the injury is above the 3rd cervical vertebra, the patient will go into respiratory arrest immediately following the injury, due to loss of nervous control of the diaphragm.

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.”

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.