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.

Imaging diagnosis conventionally begins with plain film radiography. Generally, AP radiographs of the shoulder with the arm in internal rotation offer the best yield while axillary views and AP radiographs with external rotation tend to obscure the defect. However, pain and tenderness in the injured joint make appropriate positioning difficult and in a recent study of plain film x-ray for Hill–Sachs lesions, the sensitivity was only about 20%. i.e. the finding was not visible on plain film x-ray about 80% of the time.

By contrast, studies have shown the value of ultrasonography in diagnosing Hill–Sachs lesions. In a population with recurrent dislocation using findings at surgery as the gold standard, a sensitivity of 96% was demonstrated. In a second study of patients with continuing shoulder instability after trauma, and using double contrast CT as a gold standard, a sensitivity of over 95% was demonstrated for ultrasound. It should be borne in mind that in both those studies, patients were having continuing problems after initial injury, and therefore the presence of a Hill–Sachs lesion was more likely. Nevertheless, ultrasonography, which is noninvasive and free from radiation, offers important advantages.

MRI has also been shown to be highly reliable for the diagnosis of Hill-Sachs (and Bankart) lesions. One study used challenging methodology. First of all, it applied to those patients with a single, or first time, dislocation. Such lesions were likely to be smaller and therefore more difficult to detect. Second, two radiologists, who were blinded to the surgical outcome, reviewed the MRI findings, while two orthopedic surgeons, who were blinded to the MRI findings, reviewed videotapes of the arthroscopic procedures. Coefficiency of agreement was then calculated for the MRI and arthroscopic findings and there was total agreement ( kappa = 1.0) for Hill-Sachs and Bankart lesions.

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.

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.

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.

In most cases of a complete tear, the aponeurosis of the adductor pollicis muscle may be interposed between the bones of the MCP joint and the torn ligament. When this condition (referred to as a Stener lesion) occurs, the adequate healing of the tear is prevented altogether. For a Stener lesion to occur, a complete tear of the ulnar collateral ligament must be present. However, the Stener lesion can occur even in the absence of a tear of the accessory collateral ligament or volar plate. The Stener lesion is present in more than 80% of complete ruptures of the UCL of the thumb.

When approaching this type of injury, the physician must first determine whether there is an incomplete rupture (or sprain) of the UCL, or a complete rupture. If the UCL is completely disrupted, the physician must then determine whether there is interposition of the adductor aponeurosis (Stener lesion), or simply a complete rupture of the UCL with anatomic or near-anatomic position. Radiographs are helpful in determining the possible presence of an avulsion fracture of the proximal phalanx insertion site of the ulnar collateral ligament. Stress examination, or one done under fluoroscopic guidance, can help determine the integrity of the ligament.

Most gamekeeper's thumb partial 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.

Following inspection and determination of the extent of injury, the basic labrum repair is as follows.

- The glenoid and labrum are roughened to increase contact surface area and promote re-growth.

- Locations for the bone anchors are selected based on number and severity of tear. A severe tear involving both SLAP and Bankart lesions may require seven anchors. Simple tears may only require one.

- The glenoid is drilled for the anchor implantation.

- Anchors are inserted in the glenoid.

- The suture component of the implant is tied through the labrum and knotted such that the labrum is in tight contact with the glenoid surface.

There is evidence in literature to support both surgical and non-surgical forms of treatment. In some, physical therapy can strengthen the supporting muscles in the shoulder joint to the point of reestablishing stability.

Surgical treatment of SLAP tears has become more common in recent years. The success rate for repairing isolated SLAP tears is reported between 74-94%. While surgery can be performed as a traditional open procedure, an arthroscopic technique is currently favored being less intrusive with low chance of iatrogenic infection.

Associated findings within the shoulder joint are varied, may not be predictable and include:

- SLAP lesion – labrum/glenoid separation at the tendon of the biceps muscle

- Bankart lesion – labrum/glenoid separation at the inferior glenohumeral ligament

- Biceps Tendon - exclusion of pulley injury

- Bone – glenoid, humerus — injury or degenerative change involving joint surface

- Anatomical variants — sublabral foramen, Buford Complex

Although good outcomes with SLAP repair over the age of 40 are reported, both age greater than 40 and Workmen's Compensation status have been noted as independent predictors of surgical complications. This is particularly so if there is an associated rotator cuff injury. In such circumstances, it is suggested that labral debridement and biceps tenotomy is preferred.

SLAP (Superior Labral Tear, Anterior to Posterior)

- "Type 1"

- Fraying of Superior Labrum

- Biceps Anchor Intact

- "Type 2"

- Superior Labrum detached

- Detachment of the Biceps Anchor

- "Type 3"

- Bucket Handle type tear of Superior Labrum

- Biceps Anchor INTACT

- "Type 4"

- Bucket Handle tear of Superior Labrum

- Extension of tear in Biceps Tendon

- Part of Biceps Anchor still INTACT

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.

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 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.

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.

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.

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.

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.

Diagnosis of tumefactive MS is commonly carried out using magnetic resonance imaging (MRI) and proton MR spectroscopy (H-MRS). Diagnosis is difficult as tumefactive MS may mimic the clinical and MRI characteristics of a glioma or a cerebral abscess. However, as compared to tumors and abscesses, tumefactive lesions have an open-ring enhancement as opposed to a complete ring enhancement. Even with this information, multiple imaging technologies have to be used together with biochemical tests for accurate diagnosis of tumefactive MS.

Tumefactive demyelination is distinguished from tumor by the presence of multiple lesions, absence of cortical involvement, and decrease in lesion size or detection of new lesions on serial imaging

Diagnostic methods vary, and are based on specific possible etiologies; however, an X-ray computed tomography scan of the face (or magnetic resonance imaging, or both) may be helpful.

Differentiation between this and SCC would be based on a history of recent trauma or dental treatment in the area.

Immunohistochemistry may aid the diagnosis. If the lesion is NS, there will be focal to absent immunoreactivity for p53, low immunoreactivity for MIB1 (Ki-67), and the presence of 4A4/p63- and calponin-positive myoepithelial cells.

Recurrence rate of solid form of tumour is lower than classic form.

MRI diagnosis is based on lesions that are disseminated in time and space, meaning that there are multiple episodes and consisting of more than one area. There are two kinds of MRI used in the diagnosis of tumefactive MS, T1-weighted imaging and T2-weighted imaging. Using T1-weighted imaging, the lesions are displayed with low signal intensity, meaning that the lesions appear darker than the rest of the brain. Using T2-weighted imaging, the lesions appear with high signal intensity, meaning that the lesions appear white and brighter than the rest of the brain. When T1-weighted imaging is contrast-enhanced through the addition of gadolinium, the open ring enhancement can be viewed as a white ring around the lesion. A more specific MRI, Fluid attenuation inversion recovery (FLAIR) MRI show the signal intensity of the brain. Subjects with tumefactive multiple sclerosis may see a reduction of diffusion of the white matter in the affected area of the brain.

Radiographs in osteoid osteoma typically show a round lucency, containing a dense sclerotic central "nidus" (the characteristic lesion in this kind of tumor), surrounded by sclerotic bone. The nidus is seldom larger than 1.5 cm.

The lesion can in most cases be detected on CT scan, bone scans and angiograms. Plain radiographs are not always diagnostic. MRI adds little to the CT findings which are useful for localisation. Radionuclide scanning shows intense uptake which is useful for localisation at surgery using a hand held detector, and for confirmation that the entire lesion has been removed.

Healing is prolonged, and usually takes 6–10 weeks. The ulcer heals by secondary intention.

Following conditions are excluded before diagnosis can be confirmed:

- Unicameral bone cyst

- Giant cell tumor

- Telangiectatic osteosarcoma

- Secondary aneurysmal bone cyst

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.

The histologic appearance is similar to mucoceles from other locations. The spilled mucin causes a granulation tissue to form, which usually contains foamy histiocytes. Ultrasound and magnetic resonance imaging may be useful to image the lesion. A small squamous cell carcinoma obstructing the Wharton duct may require clinical examination to be distinguished from a ranula.

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.