After an anterior shoulder dislocation, the risk of a future dislocation is about 20%. This risk is greater in males than females.

The incidence of Hill–Sachs lesion is not known with certainty. It has been reported to be present in 40% to 90% of patients presenting with anterior shoulder instability, that is subluxation or dislocation. In those who have recurrent events, it may be as high as 100%. Its presence is a specific sign of dislocation and can thus be used as an indicator that dislocation has occurred even if the joint has since regained its normal alignment. The average depth of Hill–Sachs lesion has been reported as 4.1 mm. Large, engaging Hill-Sachs fractures can contribute to shoulder instability and will often cause painful clicking, catching, or popping.

The decisions involved in the repair of the Hill–Sachs lesion are complex. First, it is not repaired simply because of its existence, but because of its association with continuing symptoms and instability. This may be of greatest importance in the under-25-year-old and in the athlete involved in throwing activities. The Hill-Sachs role in continuing symptoms, in turn, may be related to its size and large lesions, particularly if involving greater than 20% of the articular surface, may impinge on the glenoid fossa (engage), promoting further episodes of instability or even dislocation. Also, it is a fracture, and associated bony lesions or fractures may coexist in the glenoid, such as the so-called bony Bankart lesion. Consequently, its operative treatment may include some form of bony augmentation, such as the Latarjet or similar procedure. Finally, there is no guarantee that associated non-bony lesions, such as a Bankart lesion, SLAP tear, or biceps tendon injury, may not be present and require intervention.

Arthroscopic repair of Bankart injuries have high success rates, with studies showing that nearly one-third of patients require re-intervention for continued shoulder instability following repair. Options for repair include an arthroscopic technique or a more invasive open Latarjet procedure, with the open technique tending to have a lower incidence of recurrent dislocation, but also a reduced range of motion following surgery.

Inferior dislocation is the least likely, occurring in less than 1%. This condition is also called luxatio erecta because the arm appears to be permanently held upward or behind the head. It is caused by a hyper abduction of the arm that forces the humeral head against the acromion. Such injuries have a high complication rate as many vascular, neurological, tendon, and ligament injuries are likely to occur from this mechanism of injury.

A Bankart lesion is an injury of the anterior (inferior) glenoid labrum of the shoulder due to anterior shoulder dislocation. When this happens, a pocket at the front of the glenoid forms that allows the humeral head to dislocate into it. It is an indication for surgery and often accompanied by a Hill-Sachs lesion, damage to the posterior humeral head.

The Bankart lesion is named after English orthopedic surgeon Arthur Sydney Blundell Bankart (1879 – 1951).

A bony Bankart is a Bankart lesion that includes a fracture in of the anterior-inferior glenoid cavity of the scapula bone.

A Stener lesion is a type of traumatic injury to the thumb. It occurs when the aponeurosis of the adductor pollicis muscle becomes interposed between the ruptured ulnar collateral ligament (UCL) of the thumb and its site of insertion at the base of the proximal phalanx. No longer in contact with its insertion site, the UCL cannot spontaneously heal.

ITBS can result from one or more of the following: training habits, anatomical abnormalities, or muscular imbalances:

Training habits

- Spending long periods of time/regularly sitting in lotus posture in yoga. Esp beginners forcing the feet onto the top of the thighs

- Consistently running on a horizontally banked surface (such as the shoulder of a road or an indoor track) on which the downhill leg is bent slightly inward, causing extreme stretching of the band against the femur

- Inadequate warm-up or cool-down

- Excessive up-hill and down-hill running

- Positioning the feet "toed-in" to an excessive angle when cycling

- Running up and down stairs

- Hiking long distances

- Rowing

- Breaststroke

- Treading water

Abnormalities in leg/feet anatomy

- High or low arches

- Supination of the foot

- Excessive lower-leg rotation due to over-pronation

- Excessive foot-strike force

- Uneven leg lengths

- Bowlegs or tightness about the iliotibial band.

Muscle imbalance

- Weak hip abductor muscles

- Weak/non-firing multifidus muscle

- Uneven left-right stretching of the band, which could be caused by habits such as sitting cross-legged

The ulnar collateral ligament is an important stabilizer of the thumb. Thumb instability resulting from disruption of the UCL profoundly impairs the overall function of the involved hand. Because of this, it is critical that these injuries receive appropriate attention and treatment.

Most gamekeeper's thumb injuries are treated by simply immobilizing the joint in a thumb spica splint or a modified wrist splint and allowing the ligament to heal. However, near total or total tears of the UCL may require surgery to achieve a satisfactory repair, especially if accompanied by a Stener lesion.

While ITBS pain can be acute, the iliotibial band can be rested, iced, compressed and elevated (RICE) to reduce pain and inflammation, followed by stretching. Massage therapy, and many of its modalities, can offer relief if symptoms arise.

Perthes lesion is variant of Bankart lesion, presenting as an anterior glenohumeral injury that occurs when the scapular periosteum remains intact but is stripped medially and the anterior labrum is avulsed from the glenoid but remains partially attached to the scapula by intact periosteum.

The lesion is associated with any damage to the antero-inferior labrum. Most commonly due to anterior shoulder dislocation. The lesion often occurs after the initial dislocation. In chronic cases there may be fibrosis and resynovialization of the labrum and periosteum.

The lesion is best identified on MR arthrography. Additional views in "ABER" (ABduction and External Rotation) of the shoulder aid in this diagnosis.

Differential diagnoses include:

- Bankart lesion

- Bankart lesion

- Alpsa lesion

- GLAD

- HAGL

- BHAGL

Treatment is surgical re-attachment of the labrum preferably via arthroscopy.

The exact cause of the condition is unknown. There is most evidence to support vascular infarction and ischemic necrosis of salivary gland lobules as a mechanism for the condition. Experimentally, local anaesthetic injections and tying of the arteries is reported to trigger the development of tissue changes similar to NS in lab rats. Factors which are thought to cause this ischemia are listed below, however sometimes there is no evident predisposing factor or initiating event.

- Trauma e.g. during intubation, or surgical procedures

- Local anesthetic injection

- Smoking

- Alcohol

- Diabetes mellitus

- Vascular disease, (e.g. arteriosclerosis)

- Pressure from a dental prosthesis

- Allergy

- Bulimia

- Infection

- Ionizing radiation

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

Nodular fasciitis, also known as nodular pseudosarcomatous fasciitis, pseudosarcomatous fasciitis, and subcutaneous pseudosarcomatous fibromatosis, is a benign soft tissue lesion most commonly found in the superficial fascia. The lesion commonly occurs in the first three decades of life. Upper extremities and trunk are the most common affected anatomical sites. Previous history of trauma may be present. Clinically and histologically, nodular fasciitis may be mistaken for a sarcoma.

The condition is rare.

The typical age range of those affected by the condition is about 23–66 years of age. It usually occurs in smokers. The male to female ratio has been reported as 1.95:1, and 2.31:1.

Because CHILD syndrome is a congenital disorder, the symptoms may be present at birth or may develop during the first few weeks of life and continue for the lifetime of the patient.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life-threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.

CHILD syndrome is a rare disorder with only 60 recorded cases worldwide thus far in literature.

An upper motor neuron lesion (also known as pyramidal insufficiency) occurs in the neural pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves. Conversely, a lower motor neuron lesion affects nerve fibers traveling from the anterior horn of the spinal cord or the cranial motor nuclei to the relevant muscle(s).

Upper motor neuron lesions occur in the brain or the spinal cord as the result of stroke, multiple sclerosis, traumatic brain injury and cerebral palsy.

Familial dysautonomia is seen almost exclusively in Ashkenazi Jews and is inherited in an autosomal recessive fashion. Both parents must be carriers in order for a child to be affected. The carrier frequency in Jewish individuals of Eastern European (Ashkenazi) ancestry is about 1/30, while the carrier frequency in non-Jewish individuals is unknown. If both parents are carriers, there is a one in four, or 25%, chance with each pregnancy for an affected child. Genetic counseling and genetic testing is recommended for families who may be carriers of familial dysautonomia.

Worldwide, there have been approximately 600 diagnoses recorded since discovery of the disease, with approximately 350 of them still living.

Until recently, nodular fasciitis have been considered a reactive process of uncertain cause. However, recent findings indicate that nodular fasciitis is a self-limited clonal neoplastic process (see below). Clinically, nodular fasciitis presents as a subcutaneous "growth" over a period of 3–6 weeks that eventually regresses. The lesion usually reaches a size of 2–3 cm. Larger lesions are unusual. Local recurrence has been described after simple surgical excision but it is rare.

Treatment usually involves surgical removal of the lesion down to the bone. If there are any adjacent teeth, they are cleaned thoroughly to remove any possible source of irritation. Recurrence is around 16%.

A number of medical reports of phimosis incidence have been published over the years. They vary widely because of the difficulties of distinguishing physiological phimosis (developmental nonretractility) from pathological phimosis, definitional differences, ascertainment problems, and the multiple additional influences on post-neonatal circumcision rates in cultures where most newborn males are circumcised. A commonly cited incidence statistic for pathological phimosis is 1% of uncircumcised males. When phimosis is simply equated with nonretractility of the foreskin after age 3 years, considerably higher incidence rates have been reported.

Others have described incidences in adolescents and adults as high as 50%, though it is likely that many cases of physiological phimosis or partial nonretractility were included.

These are the neural tracts which descend in the ventral horn of the spinal cord, carrying signals for voluntary movement of skeletal muscle. From their origin in the primary motor cortex, these nerves pass via the corona radiata to gather in the internal capsule before crossing over to the opposite side (decussation) in the medullary pyramids and proceeding down the spinal cord to meet lower motor neurons in the anterior grey column.