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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.
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.
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.
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
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 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.
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.
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 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.
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.
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.
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.
Pharmacologic treatments for MS include immunomodulators and immunosuppressants which reduce the frequency and severity of relapses by about 35% and reduce the lesion growth. Unfortunately they are mainly tested for RRMS and its effect in tumefactive lesions is unknown. The main ones are Interferon beta (IFN-beta), Glatiramer acetate and Mitoxantrone
Plasma exchange has been reported to work at least in some cases
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.
Typical tumefactive lesions have been found to be responsive to corticosteroids because of their immunosuppressive and anti-inflammatory properties. They restore the blood-brain barrier and induce cell death of T-cells.
No standard treatment exists, but practitioners seem to apply intravenous corticosteroids, followed by plasmapheresis and cyclophosphamide in non-responsive cases High dose intravenous corticosteroids (methylprednisolone 1 g for 3–5 days) followed by oral tapering hasten clinical and radiological improvement in approximately 80% of patients
Plasmapheresis has been reported to work even in the absence of response to corticosteroids
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.
The most common finding is oculomotor nerve dysfunction leading to ophthalmoplegia. This is often accompanied by ophthalmic nerve dysfunction, leading to hypoesthesia of the upper face. The optic nerve may eventually be involved, with resulting visual impairment.
Healing is prolonged, and usually takes 6–10 weeks. The ulcer heals by secondary intention.
Curettage is performed on some patients, and is sufficient for inactive lesions. The recurrence rate with curettage is significant in active lesions, and marginal resection has been advised. Liquid nitrogen, phenol, methyl methacrylate are considered for use to kill cells at margins of resected cyst.
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
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.
Recurrence rate of solid form of tumour is lower than classic form.
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.