A Hill–Sachs lesion, or Hill–Sachs fracture, is a cortical depression in the posterolateral head of the humerus. It results from forceful impaction of the humeral head against the anteroinferior glenoid rim when the shoulder is dislocated anteriorly.

The lesion is associated with anterior or posterior shoulder dislocation. When the humerus is driven from the glenohumeral cavity, its relatively soft head impacts against the anterior edge of the glenoid. The result is a divot or flattening in the posterolateral aspect of the humeral head, usually opposite the coracoid process. The mechanism which leads to shoulder dislocation is usually traumatic but can vary, especially if there is history of previous dislocations. Sports, falls, seizures, assaults, throwing, reaching, pulling on the arm, or turning over in bed can all be causes of anterior dislocation.

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.

Posterior dislocations are uncommon, and are typically due to the muscle contraction from electric shock or seizure. They may be caused by strength imbalance of the rotator cuff muscles. Patients typically present holding their arm internally rotated and adducted, and exhibiting flattening of the anterior shoulder with a prominent coracoid process.

Posterior dislocations may go unrecognized, especially in an elderly patient and in the unconscious trauma patient. An average interval of 1 year was noted between injury and diagnosis in a series of 40 patients.

In over 95% of shoulder dislocations, the humerus is displaced anteriorly. In most of those, the head of the humerus comes to rest under the coracoid process, referred to as sub-coracoid dislocation. Sub-glenoid, subclavicular, and, very rarely, intrathoracic or retroperitoneal dislocations may also occur.

Anterior dislocations are usually caused by a direct blow to, or fall on, an outstretched arm. The patient typically holds his/her arm externally rotated and slightly abducted.

A Hill-Sachs deformity is an impaction of the head of the humerus left by the glenoid rim during dislocation. Hill-Sachs deformities occur in 35%-40% of anterior dislocations. They can be seen on a front-facing X-ray when the arm is in internal rotation. Bankart lesions are disruptions of the glenoid labrum with or without an avulsion of bone fragment.

Damage to the axillary artery and axillary nerve (C5,C6) may result. The axillary nerve is injured in 37% making it the most commonly injured structure with this type of injury. Other common, associated, nerve injuries include injury to the suprascapular nerve (29%) and the radial nerve (22%). Axillary nerve damage results in a weakened or paralyzed deltoid muscle and as the deltoid atrophies unilaterally, the normal rounded contour of the shoulder is lost. A patient with injury to the axillary nerve will have difficulty in abducting the arm from approximately 15° away from the body. The supraspinatus muscle initiates abduction from a fully adducted position.

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.

The diagnosis is usually initially made by a combination of physical exam and MRI of the shoulder, which can be done with or without the injection of intraarticular contrast. The presence of contrast allows for better evaluation of the glenoid labrum.

ITBS symptoms range from a stinging sensation just above the knee joint, to swelling or thickening of the tissue in the area where the band moves over the femur. The stinging sensation just above the knee joint is felt on the outside of the knee or along the entire length of the iliotibial band. Pain may not occur immediately during activity, but may intensify over time. Pain is most commonly felt when the foot strikes the ground, and pain might persist after activity. Pain may also be present above and below the knee, where the ITB attaches to the tibia. It will also hurt if you twist your knee to turn a corner.

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.

Iliotibial band syndrome (ITBS) is a common injury to the knee, generally associated with running, cycling, hiking or weight-lifting (especially squats).

CS Campbell, an orthopedic surgeon, originally coined the term "gamekeeper's thumb" in 1955, after he observed this condition in a number of Scottish gamekeepers. The injury appeared to occur as a result of the particular manner in which they killed small animals such as rabbits. Specifically, the animals were placed on the ground, and their necks were broken as the gamekeeper exerted downward pressure with the thumb and index fingers. This maneuver would place a valgus force upon the abducted metacarpophalangeal (MCP) joint. Over time, this would lead to insufficiency of the ulnar collateral ligament of the thumb, a condition which Campbell referred to as "gamekeeper's thumb".

In 1962, Bertil Stener described a lesion which he observed to occur in a subset of patients suffering from gamekeeper's thumb. In these patients, the distal attachment of the UCL was traumatically avulsed from its site of insertion at the base of the proximal phalanx of the thumb. The severed end of the ligament would become trapped under the aponeurosis of the adductor pollicis muscle and therefore be unable to return to its proper anatomic position. Consequently, the severed ligament would fold on itself and thus be prevented from healing and restoring stability to the MCP joint.

For a Stener lesion to occur, both the proper and accessory collateral ligaments of the thumb must be completely ruptured. The Stener lesion is present in more than 80% of complete ruptures of the UCL of the thumb.

Changes in muscle performance can be broadly described as the upper motor neuron syndrome. These changes vary depending on the site and the extent of the lesion, and may include:

- Muscle weakness. A pattern of weakness in the extensors (upper limbs) or flexors (lower limbs), is known as 'pyramidal weakness'

- Decreased control of active movement, particularly slowness

- Spasticity, a velocity-dependent change in muscle tone

- Clasp-knife response where initial higher resistance to movement is followed by a lesser resistance

- Babinski sign is present, where the big toe is raised (extended) rather than curled downwards (flexed) upon appropriate stimulation of the sole of the foot. The presence of the Babinski sign is an abnormal response in adulthood. Normally, during the plantar reflex, it causes plantar flexion and the adduction of the toes. In Babinski's sign, there is dorsiflexion of the big toe and abduction of the other toes. Physiologically, it is normally present in infants from birth to 12 months. The presence of the Babinski sign after 12 months is the sign of a non-specific upper motor neuron lesion.

- Increased deep tendon reflex (DTR)

- Pronator drift

The condition most commonly is located at the junction of the hard and soft palate. However, the condition may arise anywhere minor salivary glands are located. It has also been occasionally reported to involve the major salivary glands. It may be present only on one side, or both sides. The lesion typically is 1–4 cm in diameter.

Initially, the lesion is a tender, erythematous (red) swelling. Later, in the ulcerated stage, the overlying mucosa breaks down to leave a deep, well-circumscribed ulcer which is yellow-gray in color and has a lobular base.

There is usually only minor pain, and the condition is often entirely painless. There may be prodromal symptoms similar to flu before the appearance of the lesion.

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.

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.

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.

Necrotizing sialometaplasia (NS) is a benign, ulcerative lesion, usually located towards the back of the hard palate. It is thought to be caused by ischemic necrosis (death of tissue due to lack of blood supply) of minor salivary glands in response to trauma. Often painless, the condition is self-limiting and should heal in 6–10 weeks.

Although entirely benign and requiring no treatment, due to its similar appearance to oral cancer, it is sometimes misdiagnosed as malignant. Therefore, it is considered an important condition, despite its rarity.

Brown-Séquard syndrome may be caused by a spinal cord tumour, trauma [such as a gunshot wound or puncture wound to the cervical (neck) or thoracic spine (back)], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. Decompression sickness may also be a cause of Brown-Séquard syndrome.

The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place.

Brown-Séquard syndrome (also known as Brown-Séquard's hemiplegia, Brown-Séquard's paralysis, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis, or spinal hemiparaplegia) is caused by damage to one half of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion. It is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850.

The most distinctive clinical feature is the absence of overflow tears with emotional crying after age 7 months. This symptom can manifest less dramatically as persistent bilateral eye irritation. There is also a high prevalence of breech presentation. Other symptoms include weak or absent suck and poor tone, poor suck and misdirected swallowing, and red blotching of skin.

Symptoms in an older child with familial dysautonomia might include:

1. Delayed speech and walking

2. Unsteady gait

3. Spinal curvature

4. Corneal abrasion

5. Less perception in pain or temperature with nervous system.

6. Poor growth

7. Erratic or unstable blood pressure.

8. Red puffy hands

9. Dysautonomia crisis: a constellation of symptoms in response to physical and emotional stress; usually accompanied by vomiting, increased heart rate, increase in blood pressure, sweating, drooling, blotching of the skin and a negative change in personality.

The acronym CHILD stands for the symptoms of the syndrome:

- CH = Congenital Hemidysplasia—One side of the body, most of the time the right side, is poorly developed. The right ribs, neck, vertebrae, etc. may be underdeveloped and the internal organs may be affected.

- I - Ichthyosiform Erythroderma—At birth or shortly after birth, there are red, inflamed patches (erythroderma), and flaky scales (ichthyosis) on the side of the body that is affected. Hair loss on the same side may also be possible.

- LD - limb defects—Fingers on the hand or toes on the foot of the affected side may be missing. An arm or leg may also be shortened or even missing.

The color of peripheral ossifying fibromas ranges from red to pink, and is frequently ulcerated. It can be sessile or pedunculated with the size usually being less than 2 cm. Weeks or months may pass by before it is seen and diagnosed.

There is a gender difference with 66% of the disease occurring in females. The prevalence of peripheral ossifying fibromas is highest around 10 – 19 years of age. It appears only on the gingiva, more often on the maxilla rather than the mandible, and is frequently found in the area around incisors and canines. The adjacent teeth are usually not affected.

Peripheral ossifying fibromas appear microscopically as a combination of a mineralized product and fibrous proliferation. The mineralized portion may be bone, cementum-like, or dystrophic calcifications. Additionally, highly developed bone or cementum is more likely to be present when the peripheral ossifying fibroma has existed for a longer period of time.

A diffuse intrinsic pontine glioma (DIPG) is a tumour located in the pons (middle) of the brain stem. The brain stem is the bottommost portion of the brain, connecting the cerebrum with the spinal cord. The majority of brain stem tumours occur in the pons and are diffusely infiltrating (they grow amidst the nerves), and therefore cannot be surgically removed. Glioma is a general name for any tumour that arises from the supportive tissue called glia, which help keep the neurons in place and functioning well. The brain stem contains all of the afferent (incoming) neurons within the spinal cord, as well as important structures involved in eye movements and in face and throat muscle control and sensation.

Signs and symptoms of GM2-gangliosidosis, AB variant are identical with those of infantile Tay-Sachs disease, except that enzyme assay testing shows normal levels of hexosaminidase A. Infantile Sandhoff disease has similar symptoms and prognosis, except that there is deficiency of both hexosaminidase A and hexosaminidase B. Infants with this disorder typically appear normal until the age of 3 to 6 months, when development slows and muscles used for movement weaken. Affected infants lose motor skills such as turning over, sitting, and crawling. As the disease progresses, infants develop seizures, vision and hearing loss, mental retardation, and paralysis.

An ophthalmological abnormality called a cherry-red spot, which can be identified with an eye examination, is characteristic of this disorder. This cherry-red spot is the same finding that Warren Tay first reported in 1881, when he identified a case of Tay-Sachs disease, and it has the same etiology.

The prognosis for AB variant is the same as for infantile Tay-Sachs disease. Children with AB variant die in infancy or early childhood.