Symptoms of gamekeeper's thumb are instability of the MCP joint of the thumb, accompanied by pain and weakness of the pinch grasp. The severity of the symptoms are related to the extent of the initial tear of the UCL (in the case of Skier's thumb), or how long the injury has been allowed to progress (in the case of gamekeeper's thumb).

Characteristic signs include pain, swelling, and ecchymosis around the thenar eminence, and especially over the MCP joint of the thumb. Physical examination demonstrates instability of the MCP joint of the thumb.

The patient will often manifest a weakened ability to grasp objects or perform such tasks as tying shoes and tearing a piece of paper. Other complaints include intense pain experienced upon catching the thumb on an object, such as when reaching into a pants pocket.

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.

Several symptoms are common but not specific:

- Dull, throbbing, ache in the joint which can be brought on by very strenuous exertion or simple household chores.

- Difficulty sleeping due to shoulder discomfort. The SLAP lesion decreases the stability of the joint which, when combined with lying in bed, causes the shoulder to drop.

- For an athlete involved in a throwing sport such as baseball, pain and a catching feeling are prevalent. Throwing athletes may also complain of a loss of strength or significant decreased velocity in throwing.

- Any applied force overhead or pushing directly into the shoulder can result in impingement and catching sensations.

Gamekeeper's thumb (also known as skier's thumb or UCL tear) is a type of injury to the ulnar collateral ligament (UCL) of the thumb. The UCL may be torn, damaged or in some cases avulsed from its insertion site into the proximal phalanx of the thumb in the vast majority (approximately 90%) of cases. This condition is commonly observed among gamekeepers and Scottish fowl hunters, as well as athletes (such as volleyballers). It also occurs among people who sustain a fall onto an outstretched hand, frequently skiers.

A SLAP tear or SLAP lesion is an injury to the glenoid labrum (fibrocartilaginous rim attached around the margin of the glenoid cavity). SLAP is an acronym for "superior labral tear from anterior to posterior".

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.

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.

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.

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.

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.

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

Orbital apex syndrome, also known as Jacod syndrome, is a collection of cranial nerve deficits associated with a mass lesion near the apex of the orbit of the eye. This syndrome is a separate entity from Rochon–Duvigneaud syndrome, which occurs due to a lesion immediately anterior to the orbital apex. Most commonly optic nerve is involved.

Jacod Syndrome is commonly associated with a tumor of the middle cranial fossa (near the apex of the orbit); but it can have several other causes.

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.

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.

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 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.

There are disturbances in sensory nerves and motor nerves and dysfunction of the autonomic nervous system at the level of the lesion or below. Therefore, the signs and symptoms depend on the area of spine involved:

- Cervical: If the upper cervical cord is involved, all four limbs may be involved and there is risk of respiratory paralysis (cervical nerve segments C3, 4, 5 innervate the abdominal diaphragm). Lesions of the lower cervical (C5–T1) region will cause a combination of upper and lower motor neuron signs in the upper limbs, and exclusively upper motor neuron signs in the lower limbs. Cervical lesions account for about 20% of cases.

- Thoracic: A lesion of the thoracic spinal cord (T1–12) will produce upper motor neuron signs in the lower limbs, presenting as a spastic diplegia. This is the most common location of the lesion,

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.

Characterized by being less than 1.5 cm in diameter, osteoid osteomas most frequently occur in young men (Male:Female ratio 3:1) and may occur in any bone of the body, most frequently around the knee but often also seen in the vertebrae, in the long bones and less commonly in the mandible or other craniofacial bones.

Severe pain typically occurs at night, but can also be constant at any time of day. The chief complaint may only be of dull pain which is non radiating and persistent throughout 24 hours but increases significantly at night. Pain tends to be relieved with NSAIDs such as ibuprofen.

The afflicted may have relatively small amounts of pain that will quickly increase in severity over a time period of 6–12 weeks. The skin temperature around the bone may increase, a bony swelling may be evident, and movement may be restricted in adjacent joints.

Spinal lesions may cause quadriplegia and patients with skull lesions may have headaches.

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.