Ankle ligament injuries

                              Ankle ligament injuries

                                                 Dr. KS Dhillon

Anatomy of ankle ligaments

The ligaments around the ankle can be divided into three groups: the lateral ligaments, the deltoid ligament on the medial side, and the ligaments of the tibiofibular syndesmosis which joins the tibia to the fibula.
1. There are three ligaments on the lateral side of the ankle that make up the lateral ligament complex. These include:

• The anterior talofibular ligament (ATFL), which connects the front of the talus to the fibula.
• The calcaneofibular ligament (CFL), which connects the calcaneus to the fibula.
• The posterior talofibular ligament (PTFL), which connects the rear of the talus to the fibula

2. The deltoid ligament supports the entire medial side of the ankle. It  has 2 components:
The superficial components which consist of:

• The tibiocalcaneal ligament,
• The talonavicular ligament
• The posterior superficial tibiotalar ligament
• The tibiospring ligament

The deep components which consist of:

• The anterior tibiotalar ligament (ATTL)
• The posterior deep tibiotalar ligament (PDTL)

3. The tibiofibular ligament (AITFL) connects the tibia to the fibula. It consists of:

• Anterior inferior tibiofibular ligament (AITFL)
• The posterior inferior tibiofibular ligament (PITFL)
• The inferior transverse ligament
• The interosseous ligament which extends from the tibia to the fibula. 

Ankle ligament injuries

The ankle is the most frequently traumatized body site and ankle injuries account for 10–30% of all sports injuries [1]. Ankle sprains are the most common musculoskeletal injuries and in all sports injuries, the rate of ankle sprains ranges from 15 to 20 % [2,3].

One inversion ankle injury occurs per 10,000 people every day which amounts to about 5000 injuries a day in the UK and about 23,000 in the US [4,5,6]. Most ankle injuries occurring during sports involve the lateral ankle ligament and this represents about 77% ankle sprains [1].

The most common mechanism of injury which leads to lateral ligament sprain or tear is a combination of inversion and adduction of the foot in plantar flexion [7]. This force injures the anterior talofibular ligament. When the inversion force occurs in a dorsiflexed ankle, the calcaneofibular ligament which is the primary stabilizer gets injured. Anterolateral rotatory instability occurs when the anterior talofibular ligament is injured and the medial ligaments are intact [8]. In addition to this, when the calcaneofibular ligament tears there is tilting of the talus [8].

Deltoid ligament injuries occur with eversion and external rotation. They are usually accompanied by fractures of the ankle [9].

Syndesmotic injuries result from forced external rotation during dorsiflexion and eversion movements of the ankle. Syndesmotic injury can occur in isolation or may be associated with ankle fractures [10].

Ankle ligament sprains are usually graded on the basis of severity of injury to the ligament [11].
In grade I injuries (mild sprain) there is a mild stretching of the ligaments without visible rupture or joint instability. The injury is usually limited to the ATFL.

 In grade II injuries (moderate sprain) there is a partial rupture of the ligament with moderate swelling and pain with functional limitations and a mild to moderate instability. Such patients typically present with problems in weight-bearing. In grade II injuries there is a tear of the ATFL with partial or complete tear of the CFL.

 In grade III injuries (severe sprain) there is a complete rupture of the ligament with marked pain, swelling, hematoma formation and a marked impairment of function with instability. This is the most severe type of injury where there is a tear of the ATFL and CFL and sometimes there is a tear of the capsule as well as a tear of the PTFL [12].

Although this classification is available and often used, there however remains clinical difficulties in quantifying the severity of these injuries.

Clinical evaluation

Patients will give a history of a twisting injury to the ankle. They will complain of pain, swelling of the ankle and of difficulty in walking.

Examination will show swelling, tenderness, and ecchymosis at the site of injury. There will be limitation of ankle movements and the walking pattern will be altered to avoid pain.

Grade I injuries will present with mild swelling, tenderness and minimal limitation of movements. In grade III injuries there will be diffuse swelling, ecchymosis, tenderness, ankle instability and inability to weight bear.

Pain, swelling, and tenderness on the medial side of the ankle with a soft tissue defect would denote a deltoid ligament injury.

Syndesmotic injury will present with tenderness over the anterior aspect of the syndesmosis and positive squeeze or external rotation test [13]. In all ankle injuries assessment of the neurovascular status is very important.

Stress testing is useful in the diagnosis of ankle ligament injuries if there is not much pain.

Useful stress tests include:

• Anterior drawer test: Anterior displacement of the talus over the tibia is carried out and displacement of more than 4mm denotes tear of the ATFL.
• Talar tilt test: A stress radiograph of the ankles is carried out by forced inversion of the ankle while the tibia is stabilized. A more than 5° of difference in outward shift as compared with the contralateral side denotes a CFL tear.
• Eversion stress test: Abduction with eversion of the ankle is carried out while the tibia is stabilized and increased laxity as compared to the opposite side denote deltoid ligament tear.
• External rotation stress test: Plantarflexion and external rotation of the ankle is carried out while the tibia is stabilized and the presence of pain and tenderness over the syndesmosis denotes syndesmotic injury.

Diagnostic studies

The usual first step following clinical examination after an ankle injury is obtaining x rays of the ankle. The Ottawa Ankle Rules (OAR) established by Stiell et al [14] help in decision making as to whether an x-ray is needed. According to the OAR, the following types of patients do not need x rays:

1. Patients who can weight-bear at the time of injury which means they are able to walk at least four steps, without assistance, two steps on the injured side and two on the other side, even if they are limping.
2. Patients are able to walk at the time of evaluation. This means walking at least four steps, without assistance two steps on each side, even if limping.
3.Absence of tenderness along the distal 6cm of the tibia or fibula (for ankle x rays).
4.Absence of tenderness on the proximal 5th metatarsal and navicular bone (for foot x-ray).


Initial ankle X-rays should include anteroposterior (AP), lateral and mortise views. AP and mortise views in dorsiflexion and plantarflexion can provide information about talar osteochondral lesions. If there is tenderness on the 5th metatarsal an oblique x-ray of the foot must be obtained.

Stress x-rays can be obtained to diagnose CFL tears. AP and lateral stress views with 20 degrees of internal rotation and valgus stress are useful in the diagnosis of deltoid ligament injuries.

On performing the valgus stress test a more than 10° of valgus tilt and/or more than 5 mm of widening in the medial clear space denotes syndesmotic injury. Other radiographic findings of syndesmotic injury include an increased tibiofibular clear space, decreased tibiofibular overlap and increased medial clear space [12].

Magnetic resonance imaging (MRI) is usually not indicated in patients with acute ankle injuries unless there is evidence of major ankle instability. MRI is often useful in patients in whom concomitant injuries such as osteochondral and tendon injuries are suspected. MRI may also be indicated in patients who have chronic ankle pain after an ankle sprain and in patients who have a clinical history of repetitive trauma and complex injuries of the ankle [12].

Treatment of ankle sprains

As with most injuries, prevention of injury is the best treatment. The best method of preventing ankle sprains remains controversial. Various types of footwear and bracing has been tried to prevent ankle sprains. Some have used low-top shoes combined with lace-up bracing while others have used high-top shoes with taping [15,16]. The use of taping has also been found to be of not much use in preventing ankle sprains [17].

The treatment of grade I and grade II ankle ligament injuries is quite straight with no controversy. The general consensus is that grade I and II injuries should be treated conservatively.
Almost all authors agree that patients who have a grade-I or grade-Il injury recover quickly with non-operative management [7,18,19,20] and that the prognosis is good or excellent in most patients [4,5,7,18,19,20,21,23,24,25].

Conservative treatment includes a short period of rest, ice, compression, and elevation (RICE) followed by protective taping or bracing and functional rehabilitation [18].

There are 4 stages of biological healing in ankle ligament injuries and functional rehabilitation treatment is based on these four stages.

In the 1st stage, there is inflammation and swelling and RICE protocol helps reduce inflammation and swelling [26]. In the 2nd phase, there is healing and proliferation with fibroblasts forming collagen fibers. In this phase bracing or taping is needed to prevent talar tilt [27]. The 3rd phase is the maturation phase when the collagen fibers mature and become scar tissue. This phase starts at about 3 weeks after the injury. Controlled stretching is started which allows reorientation of collagen fibers which prevents stiffness [28].

The 4th and final stage of healing occurs between 6 to 8 weeks following the injury. At this stage, the patient returns to near full strength and can return to full activity. Full recovery can take up to 6 to 12 months [28].

Functional rehabilitation involves ankle mobilization, muscle strengthening and improving proprioception. A stationary bicycle can be used for increasing range of motion. Tilt board and trampoline can be used to improve proprioception [28]. Nonsteroid anti-inflammatory medications and cryotherapy have only short term benefits.

The average disability period for grade I injuries is about 8 days and the average disability period for grade II injuries is about 15 days [23].

Treatment of grade III ankle sprains is less standardized and more controversial. Good results have been reported for grade III ankle ligament tears with acute surgical repair, cast immobilization, and also with functional rehabilitation.

Kannus and Renstrom [30] were one of the earliest authors to conclude that functional treatment is the preferred method for treatment of complete tears of lateral ligament. Their findings have since been corroborated by other researchers [31,32].

Kannus and Renstrom [30] carried out a review of 12 prospective studies
and found that functionally treated patients returned to work 2 to 4 times faster than those who had acute repair.

Kaikkonen et al [33] carried out another comparative study and reported excellent to good outcomes in 87% of functionally treated patients as compared to surgically treated patients where only 60% of patients had good to excellent outcome. Furthermore, the range of ankle movements at final follow up was less in patients who had surgery.

Munk et al [34] carried out a prospective study to compare the long term outcome of three methods of treatment of lateral ligament injuries. The methods of treatment included, operation and walking-cast for 5 weeks, walking-cast alone, and elastic bandage. They followed up the patients for an average period of 11 (9-13) years. They found that the residual disabilities and late complications, such as instability, pain on activity, talocrural arthrosis and the number of ligament reconstructions were equally low in all 3 groups. They concluded that nonoperative treatment is adequate for lateral ligament tears.

Surgical repair of acute ankle ligament tears is rarely performed. There are some proponents of acute repair for lateral ankle sprains. Leach and Schepsis advocated primary repair of grade III tears in young athletes with Grade III sprains [35]. A study by Pijnenburg et al [36] found better objective scores in patients who had surgical repair of the ligament but they concluded that in most patients surgery was not worth the additional cost, risks, and complications.

Surgery is not indicated in the acute setting and if any late instability develops, the instability can be treated by surgery with a similar outcome as with a primary repair [30].

Kerkhoffs et al [37] carried out a Cochrane systematic review to find out if primary surgical repair of the torn ankle ligament gives a better result as compared to conservative treatment. They concluded that there was not enough evidence from randomised controlled trials to show that surgery gives a better result than conservative treatment for acute ankle sprain in adults.

Complications

Risk of reinjury

Attenborough et al [38] carried out a systematic search of the literature to determine the presence of common aspects of chronic ankle instability (CAI) within individual sports. They found that in volleyball the incidence of recurrent sprains was 46%, in American football 28%, in basketball 19% and in soccer the incidence was 11%. Other researchers have found the incidence of recurrent sprains to vary from 12% to 47% [39,40,41,42,43].

A history of lateral ankle sprain is one of the strongest risk factors for a future lateral ankle sprain [44,45,46].
Future injury-prevention interventions must keep in mind the risk for
subsequent injury after an initial ankle sprain.

Chronic ankle instability(CAI)

The high reinjury rates after an acute lateral ankle sprain are associated with the development of CAI. CAI is characterized by ongoing pain, giving way and feelings of instability in the ankle. This leads to persistent disability when the instability interferes with daily activities. Chronic ankle instability can develop after an acute ankle sprain, from multiple injuries to the same ligament.

Chronic ankle instability can be due to mechanical instability, functional instability, or a combination of both. Mechanical instability can be due to pathologic laxity, arthrokinematic changes, synovial irritation, or osteoarthritis. Functional instability is usually caused by insufficiencies in proprioception and neuromuscular control [47].

A recent review of CAI by Gribble et al [48] suggested that up to 70% of individuals who sustain an acute lateral ankle sprain may develop CAI over a short time period following the initial injury.
Doherty et al [49] in a prospective cohort study found a 40% CAI prevalence rate at one year after a first-time lateral ankle sprain.

CAI prevalence is higher in individuals who participate in running, jumping, and cutting activities. Individuals who participate in dance and gymnastics have a higher prevalence of CAI than other sporting populations [38,48].

CAI is treated with nonoperative measures such as peroneal strengthening, lateral heel wedges, proprioceptive training, and strapping or bracing [28]. Patients who have functional instability without demonstrable mechanical instability will benefit from these non-operative measures. Patients with mechanical instability who do not respond to conservative treatment over a period of about 6 months can be treated with surgery.

Surgery for CAI can be carried out by an anatomic repair, nonanatomic reconstruction, or an anatomic reconstruction of the lateral ligament.

Brostrom first described the technique of an anatomic mid-substance repair of the ATFL and CFL in 1966 [50]. In Broström’s anatomic repair, midsubstance imbrication and suture of the ruptured ligament ends is carried out.

Gould et al [51] modified the Brostrom procedure. They reinforced the repair using the lateral talocalcaneal ligament and the inferior extensor retinaculum to correct the subtalar instability. Karlsson et al [52] imbricated the damaged ligaments and reinserted the ligaments through drill holes in the fibula.

Over the years several non-anatomic reconstruction methods have been described. The first was by Elmslie in 1934. Elmslie used a fascia lata graft to reconstruct the lateral ankle ligaments [53].

Watson-Jones in 1952 popularised the use of the peroneus brevis tendon to reconstruct the lateral side of the ankle by rerouting the tendon in a posterior to anterior fashion through the fibula and securing it onto the talar neck [54].

Evans in 1953 reported a simplified modification of the Watson-Jones procedure where he routed the peroneus brevis tendon obliquely through the distal fibula in an anterodistal to the posterioproximal fashion [55]. Chrisman and Snook [56] modified the original Elmslie procedure. He split the peroneus brevis tendon and transferred one portion of the tendon through the fibula and into the calcaneus, thus providing a much more anatomic reconstruction.

Anatomic reconstructions can augment anatomic repair without sacrificing lateral ankle kinematics. Colville used a split peroneus brevis tendon to augment a repaired ATFL and CFL. In this anatomic reconstruction, the peroneus brevis is placed into the anatomic origins and insertions of the lateral ligaments. As a result, normal ankle kinematics and subtalar motion are maintained [57]. In anatomic reconstructions, free autograft or allograft tendons such as the gracilis, fascia lata, plantaris, palmaris, and semitendinosus can also be used. This technique is indicated in patients with poor tissue quality and for revision surgery.

Posttraumatic Osteoarthritis 

Posttraumatic osteoarthritis (PTO)  is one of the more serious complications of ankle sprains. The incidence of PTO after lateral ankle sprains varies between 13% to 22% and 80% of ankle PTO cases are due to ankle sprains [48]. Besides ankle sprains, the other causes of ankle PTO include fractures and osteochondral lesions [58].

Fifty percent of the PTO develop after a single acute sprain and the other 50% develop as a result of recurrent sprains [48].

A retrospective study by Valderrabano et al [58] showed that the overall mean latency time for symptomatic end-stage ligamentous posttraumatic ankle osteoarthritis was 34.3 years (range, 6-57 years). They also found that ankles that were treated surgically a shorter mean latency time as compared to those who were treated nonoperatively.

In a 20-year follow-up study, Lofvenberg et al [59] found a 13% incidence radiographic OA in patients CAI. 

Canale and Belding [60] found a much higher incidence of posttraumatic OA in patients with CAI. They found an incidence of 48% at 11 years follow up.

The presence of degenerative changes on arthroscopic examination of the ankle are higher with reports demonstrating degenerative changes in 21% to 95% percent of patients with CAI [ 48].
The exact aetiology of these degenerative changes has not yet been established. Taga et al [61] carried out preoperative arthroscopy of the ankle in 31 patients before ligament operation. Nine patients had a fresh injury, and 22 patients had chronic injuries. They found chondral lesions in 89% of the freshly injured ankles and 95% of the ankles with chronic injuries. The authors were of the opinion that acute LAS may be sufficient to cause an osteochondral lesion. These findings could explain why patients with a single episode of ligament injury can develop post-traumatic osteoarthritis
.
There is a scarcity of literature on the interaction of symptoms with documented degenerative changes in the ankle following LAS. Van Ochten et al [62] carried out a study to look at the correlation between degenerative changes in ankle and symptoms. Their study included 206 patients who had an ankle sprain 6 to 12 months before the study. The patients filled up a standard questionnaire and had a physical examination, x rays and MRI of the ankle. Of the 206 patients, 98 had persistent complaints of pain and 108 did not have any complaints. There were no significant differences in structural abnormalities between patients who had symptoms and those who did not have any symptoms. In both groups, many structural abnormalities were found on x rays and MRI. X rays showed OA in the talocrural joint in 45.1% of patients and 36.5% of the patients had talonavicular sclerosis. On MRI bone oedema was seen in 33.8% of the patients and talocrural osteophytes in 39.5% of the patients. Talonavicular osteophytes were seen in 54.4%, sclerosis in 47.2%, and osteoarthritis in 55.4% of the patients. They also found anterior tibiofibular ligament damage in 16.4% of the patients.

They concluded that the prevalence of structural abnormalities is high on radiography and MRI in patients with a previous ankle sprain and there is no difference in structural abnormalities in patients with and without persistent complaints. They were of the opinion that imaging alone will not provide the explicit reason for the persistent complaints after LAS.

Conclusion

Ankle sprains are the most common sporting injury (15% to 20% of all sporting injuries). Seventy-seven percent of all ankle sprains involve the lateral ligamentous complex. Approximately 20 percent of acute ankle sprains result in functional or mechanical instability leading to chronic ankle instability.

Diagnosis is made through a thorough history and a good clinical examination. Radiographs and MRI are useful for excluding other associated pathologies.

There are 3 grades of ankle sprains. Grade I and II sprains are always treated conservative. Treatment of grade III sprains is more controversial. The consensus is that grade III sprains should be treated conservatively in the acute phase. Late instability with persistent symptoms can be treated surgically. Anatomical repairs are most commonly used for the treatment of symptomatic chronic instability of the ankle.

Complications after ankle sprains are not uncommon. There is a high risk of re-injury after ankle sprains, especially in athletes. Other disabling complications include chronic ankle instability and posttraumatic OA.

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Arthrofibrosis of the knee

                                   Arthrofibrosis of the knee

                                          Dr KS Dhillon

What is arthrofibrosis of the knee?

Spraque et al [1] were the first to describe knee arthrofibrosis in 1982. Arthrofibrosis refers to the development of excessive fibrotic tissue or adhesions within and around a joint which leads to limitation of movements of the joint. In the knee, the adhesions occur anteriorly in the infrapatellar fat pad, the pretibial recess, the suprapatellar pouch, medial and lateral gutters, posteromedial and posterolateral capsule. The clinical spectrum of this varies widely, ranging from localized to diffuse involvement of all compartments of the knee and of the extra-articular soft tissues around the knee.

Etiology of knee arthrofibrosis

There are several causes of knee arthrofibrosis and these include:

1.Soft-tissue Injury

The severity of soft-tissue injury, multi-ligamentous injury, severity of bony injury and dislocations of the knee, all play a role in the pathogenesis of arthrofibrosis.

2.Infection

Knee infections lead to the production of intraarticular inflammatory mediators which in turn produce synovitis and toxic degeneration of the articular surface. Local cytokine activation leads to fibrous scar formation.

3.Knee joint immobilization

Knee immobilization for ligament and bony injury as well as immobilization following knee surgery is a well-established risk factor for arthrofibrosis.

4.Timing of Surgery

Acute knee injuries need to be treated on admission to the hospital. Reconstructive surgery should be delayed until recovery from the acute injury has occurred. Timing of reconstructive surgery of the knee remains controversial. Majority of the authors recommend a delayed reconstruction of knee ligaments at 3 weeks. This delayed allows time for soft-tissue healing, resumption of full ROM, and improved strength. Reconstruction of knee ligament in the acute phase is associated with an increased incidence of arthrofibrosis [2,3,4].

5.Extra-articular and intraarticular procedures

Open arthrotomy and periarticular operative procedures such as collateral ligament repair as well as capsular surgery are known to cause arthrofibrosis. Multiple ligament reconstruction of the knee is also a known risk factor for arthrofibrosis. Graft malposition during ligament reconstruction can also lead to arthrofibrosis.

6.Genetic risk factors

Some patients develop arthrofibrosis despite efforts to reduce or eliminate the aforementioned risk factors. This has led some researchers to believe that there may be some genetic predisposition to arthrofibrosis after injury.

7.Complex regional pain syndrome

Complex regional pain syndrome also known as reflex sympathetic dystrophy inhibits effective patient participation in proper postoperative rehabilitation. As a result of the pain, quadriceps inhibition occurs leading to muscle atrophy and reduced joint mobility which in turn leads to arthrofibrosis.

Pathophysiology of arthrofibrosis

Locally acting growth factors and cytokines signals, control tissue organization and homeostasis in the human body. The cytokines coordinate cell growth, differentiation, and programmed cell death. This is done through constant signals which are sent between local cells (paracrine) and among themselves (autocrine). Platelets release transforming growth factor-β (TGF-β) and this growth factor plays an important role in tissue repair [5]. At the site of injury, the growth factor
initiates a series of events that result in the production of extracellular matrix proteins and protease inhibitors. Proteolytic enzyme production is also inhibited. An increase in the concentration of extracellular matrix at the site of injury results in TGF-β feedback inhibition. Excessive expression of TGF-β results in progressive deposition of matrix and tissue fibrosis [6].

Clinical presentation

Patients with arthrofibrosis of the knee can present with knee stiffness, pain, limping, warmth, swelling, crepitus, and/or weakness [7]. Loss of motion is the main symptom of knee arthrofibrosis. There can be a loss of flexion, loss of extension or loss of both flexion and extension.
Shelbourne et al [8] described a classification system based on the pattern of knee stiffness.

• Type I. Patients have normal flexion and less than 10-degree extension loss.
• Type II. Patients have normal flexion and more than10-degree extension loss.
• Type III. Patients have more than a 10-degree extension loss and a more than a 25-degree flexion loss with patella tightness.
• Type IV. Patients have an extension loss of more than 10 degrees and 30 degrees or more loss of flexion with patella infera with marked patella tightness.

Del Pizzo et al [9] classified knee arthrofibrosis based on deviation from full extension and amount of flexion present:

• Mild: less than 5° loss of extension, flexion more than 110° 
• Moderate: 5°–10° loss of extension, flexion between 90°–100° 
• Severe: More than 10° loss of extension, flexion less than 90° 

Paulos et al [10] were the first to describe infrapatellar contraction syndrome (IPCS). In patients with IPCS, there is a significant reduction of both flexion (>25°) and extension (>10°) with a decrease in patellar mobility which is characterized as patellar entrapment. IPCS is caused either by an exaggerated pathologic fibrous hyperplasia of the anterior soft tissues of the knee or certain risk factors associated with knee surgery such as poor graft isometry, joint immobilization, and muscle weakness.

Paulos et al [10] divided patients with IPCS into three stages namely the prodromal, active, and residual stages.

In the prodromal stage, there is periarticular inflammation, oedema, weakness of the quadriceps, extension lag, painful movements and tenderness over the patellar tendon with decreased patellar excursion.

In the active stage, there is a marked decrease in patellar mobility, severe quadriceps atrophy, worsening knee motion, and induration of the fat pad with a rigid patellar tendon.

In the residual stage, the peripatellar and retinacular tissues are more
supple than in the active stage and there is marked quadriceps atrophy with loss of knee flexion and extension.

The diagnosis of joint arthrofibrosis is clinical. It is made after excluding other causes of knee stiffness. There are no radiological investigations which can confirm the diagnosis. Arthroscopy can confirm the diagnosis but it is not warranted for diagnosis. Tissue biopsy is also not required to make the diagnosis.

The average genu recurvatum is 5 degrees for males and 6 degrees for females, and the average knee flexion is 140 degrees for males and 143 degrees for females [11]. Studies have shown that 67 degrees of knee flexion is required in the swing phase of walking, 83 degrees to ascend stairs, 90 degrees to descend stairs, and 93 degrees to rise from a standard chair [12]. Loss of knee flexion is usually better tolerated than the loss of knee extension. Even small discrepancies in extension are associated with increased energy consumption during gait and extension loss can cause undue strain on the quadriceps musculature and the patellofemoral joint [13].

Ligament reconstruction is probably the most common cause of arthrofibrosis. The incidence of knee stiffness after ligament reconstruction varies between 4% to 35% [14]. Shapiro and Freedman [15] reported a 57% incidence of knee motion loss in patients undergoing combined anterior cruciate ligament and posterior cruciate ligament reconstructions.

IPCS is the most serious form of arthrofibrosis which can complicate ligament reconstructions. The natural history of an anterior cruciate ligament-deficient knee is much more benign than the natural history of a knee that develops IPCS [10].

Treatment of knee arthrofibrosis

1.Immediate Postoperative Motion

Following knee ligament injury and knee surgery, all efforts must be directed at prevention arthrofibrosis and consequent loss of motion. Prolonged immobilization should be avoided and immediate active and passive range of motion exercises should be started.

Noyes et al [16] was able to show a good outcome with postoperative immediate knee motion and early intervention in patients who had ACL reconstruction. In a prospective study, 93% (413 of 443) of their patients regained full ROM (0º to 135º) with the use of active and passive knee exercises in the immediate postoperative period. Of the 30 patients who did not regain full range of movements, 23 were subjected to a postoperative treatment regime which included hyperflexion and hyperextension exercises and serial extension casting. Eight patients who did not respond to cryotherapy, NSAIDs, elevation, and compression were given oral steroids. In refractory cases, manipulation under anesthesia, physical therapy, and arthroscopic débridement were performed. At the end of treatment, 98% of their patients regained full knee motion, 2% had minor extension limitations, less than 1% required arthroscopic release of adhesions, and no patient developed permanent arthrofibrosis.

2.Postoperative Knee Bracing

A rehabilitation brace is commonly used after ACL reconstruction although its use is controversial. Majority of the surgeons use a brace for about 4 weeks after ACL reconstruction [17].

Melegati et al [18] carried out a prospective study to assess the role of the rehabilitation brace in restoring knee extension after anterior cruciate ligament reconstruction. They compared the outcome in two groups of patients. In one group the knee was braced from 0° to 90° and in the other group the knee was locked in full extension during the first week after ACL reconstruction. They found that patients who were braced in full extension for the first week postoperatively had a lower heel-height
differences at 4 and 8-week followup as compared to patients whose brace was unlocked twice daily for physiotherapy.

Mikkelsen et al [19] in a randomized prospective study showed that patients braced in 5 degrees hyperextension had less extension deficits as compared to patients whose knee was immobilized in full extension (0°) after ACL reconstruction. The outcome was measured 3 months after the surgery. The authors concluded that the use of a knee brace in hyperextension for at least 3 weeks after ACL reconstruction is an effective way of preventing postoperative extension loss.

3.Manipulation of knee under anesthesia

Dodds et al [20] reported the results of knee manipulations in 42 knees which had persistent flexion or extension deficits after ACL reconstruction. The manipulation was done at an average of 7 months (range, 3 to 14 months) following the reconstruction and the average follow up was 26 months (range, 6 to 56 months). After manipulation, the average flexion was increased from 95 degrees to 136 degrees and average extension from 11 degrees to 3 degrees. The outcome after manipulation was proportional to the severity of extension loss before manipulation. Patients with greater extension deficits achieved less overall final extension. They were able to achieve improvement in both flexion and extension in 86% of the knees. The authors of this study recommended manipulation within 12 weeks of ACL reconstruction. There are other authors who recommend manipulation within 4 to 12 weeks of reconstruction. Overaggressive and significant delay in manipulation can result in complications such as chondral damage, distal femur or patella fracture, patellar tendon rupture, quadriceps myositis ossificans and ossification of the MCL.

Consensus has been reached that MUA should be carried out between three and six months post-operatively and MUA is not indicated after 6 months [21].

4. Surgical treatment

A.Arthroscopic treatment

Arthroscopic debridement or arthrolysis is often successful in treating arthrofibrosis. The procedure can be carried out on an outpatient basis. A careful and thorough inspection of all compartments is carried out.

First, the suprapatellar pouch is cleared of adhesions followed with the medial and lateral gutters. The infrapatellar fat pad is then debrided and the recess between the patellar tendon and anterior tibia be reestablished.

In patients with excessive scarring and patellar entrapment, the medial and lateral retinacula are released.

In patients with limitation of extension clearance of the notch and notchplasty will be necessary. In some patients with limitation of extension, posteromedial and posterolateral capsular release may be necessary.

Aglietti et al [22] carried out a prospective study of 31 knee arthrolysis which were performed for loss of motion after anterior cruciate ligament reconstruction. The arthrolysis was carried out at an average of 10.6 months after the reconstruction (range 4-25 months). Twenty-one knees had arthroscopic and 10 had open surgery. In most knees suprapatellar, medial, and lateral gutter adhesions were removed and in 7 knees posteromedial and/or posterolateral capsulotomy was necessary. The ACL graft was nonfunctional and malpositioned in 19 knees.

The average follow up after arthrolysis was 3.5 years (range 1.5-7). Satisfactory outcome was obtained in only 37% of the knees. The authors found that arthrolysis performed within 8 months from index operation had a better outcome.

Cosgarea et al [23] carried out a retrospective analysis of 43 knees in 37 patients who had previous ligament surgery and developed postoperative arthrofibrosis. The average follow up was 3.6 years. Arthrolysis was carried out when there was flexion or extension deficits of equal to or more than 10 degrees or when motion failed to improve despite 2 months of intense therapy. Though flexion improved from 83% to 97% of the contralateral side and extension deficits improved from 14 degrees to 3 degrees, only 62% achieved satisfactory functional results. They found that lysis carried out sooner then 6 months had a better outcome.

Fisher et al [24] reported good outcome of arthroscopic excision of abundant tissue in the anterior tibiofemoral joint which caused an extension block after open ACL reconstruction. They had forty-two patients in their series and all patients had marked improvements in function and symptoms especially in activity-related anterior knee pain, crepitus at terminal extension, and knee stiffness.
Klein et al [25] reported the outcome of arthroscopic management of postoperative arthrofibrosis in 46 knees. The gain in range of motion was excellent in 54.5%, good in 21.7%, and fair and poor in 23.8%. Reduction of pain occurred in 80.4% of the patients. Patient satisfaction was excellent or good in 56.5%, fair in 39.1% and poor in 4.3%of the patients.

B.Open Debridement and Soft Tissue Release

Open debridement and soft tissue release is sometimes required in patients with severe scarring and in patients who have failed less-invasive approaches. Open surgery is usually required in patients with chronic motion problems who have long-standing extension deficits and generalized arthrofibrosis. In such patients, open surgery is usually a salvage procedure [26].

When extensive extra-articular calcification is present, open excision has to be carried out to restore knee motion. When extensive intra-articular fibrosis is present an anteromedial approach is used to completely debride all fibrous scar tissue anteriorly and posteriorly in the joint. Sometimes lateral retinacular release is needed to mobilize the patella. Following the surgery meticulous hemostasis has to be achieved to prevent a postoperative hematoma, which can lead to arthrofibrosis.

Millett et al [26] carried out a retrospective review of eight knees in 8 patients who had open debridement soft tissue release for extensive intraarticular and periarticular fibrosis of the knee. The average preoperative range of motion was 62.5° (flexion 81°, loss of extension 18.8°). The motion improved to an average of 124° after surgery. The average flexion improved from 81° to 125° and the loss of extension improved from 18.8° to 1.25°. Functional outcome was good and patient satisfaction was high.

Lobenhoffer et al [27] carried out a prospective study of 24 patients who were treated with arthroscopic arthrolysis and open posterior capsulotomy for flexion contractures of the knee. Twenty-one patients were available for review with a mean follow-up of 18 months (range 6–38 months). The mean preoperative extension deficit was 17° (range 10–30°). The postoperative extension improved to a mean value of 2°. None of the patients had more than 5° of extension deficit at follow-up. The knee function improved significantly with a Lysholm Score 62 preoperatively and 88 postoperatively 88 and the Tegner Scale 2.2 preoperatively and 4.0 postoperatively.

Tardy et al [28] carried out a retrospective study to assess the outcome arthroscopic anterior debridement and open posterior medial and lateral capsular release in twelve patients who presented with a chronic flexion contracture of 10° or more after ACL reconstruction. The average follow-up period was 38months (range 6 to 90 months). All patients except one (93%) achieved complete extension. Only one patient (7%) had a residual postoperative flexion deformity of five degrees. The range of motion improved significantly after arthrolysis. There were no postoperative complications. The post-operative objective IKDC scores, subjective IKDC scores, Knee injury and Osteoarthritis Outcome Score (KOOS), pain score, symptoms scores, ADL scores, sports activities scores and quality of life scores all improved. The mean patients' satisfaction was 9.25±0.6 (SD) out of 10 after arthrolysis.

The authors concluded that open posterior release with both posteromedial and posterolateral approaches is a safe and efficient procedure in patients with persistent flexion contracture.
Wierer et al [29] carried out a study to evaluate the efficiency of an arthroscopic posterior capsule release for the treatment of persistent knee extension deficits following ACL reconstruction. The study included 10 patients with knee flexion contracture who had arthroscopic debridement and arthroscopic posterior capsular release.

The median follow-up period was 25months (range: 14 to 69months). The median preoperative extension deficit was 15° (range: 10 to 20°) and the median postoperative extension deficit was one degree (range: 0 to five degrees). The median Lysholm score improved from 52 (range: 32 to 67) to 92 (range: 84 to 100) postoperatively. The median Tegner Activity Level improved from three to six postoperatively. The median VAS status for pain decreased from five to one. There were no postoperative complications.

The authors concluded that arthroscopic posterior capsulotomy is a safe and effective procedure for treatment of knee flexion contractures.

Conclusion

Arthrofibrosis, the formation of extra and intra-articular excessive fibrotic tissue can result from knee injury, infection, extra and intra-articular surgical procedures, and joint immobilization.
Arthrofibrosis can present with knee stiffness, pain, limping, warmth, swelling, crepitus, and/or weakness. Loss of motion remains the main symptom of knee arthrofibrosis. Several classification systems for arthrofibrosis based on the pattern of knee stiffness are available.
Every effort should be taken to prevent arthrofibrosis because loss of knee movements especially extension can be very disabling. Several treatment options are available including knee mobilization exercises, bracing and manipulation of the joint under anesthesia. Failure of noninvasive treatment will warrant surgical treatment which includes arthroscopic or open arthrolysis and soft tissue release. The outcome of treatment is variable. Some of the older studies reported outcome of treatment which was not so good but some newer studies show a much better outcome of treatment.

References

1. Spraque NF, O’Connor RL, Fox JM. Arthroscopic treatment of postoperative knee arthrofibrosis. Clin Orthop. 1982;166:165-172.
2. Shelbourne KD, Wilckens JH, Mollabashy A, DeCarlo M: Arthrofibrosis in acute anterior cruciate ligament reconstruction: The effect of timing of reconstruction and rehabilitation. Am J Sports Med 1991;19:332-336.
3. Wasilewski SA, Covall DJ, Cohen S: Effect of surgical timing on recovery and associated injuries after anterior cruciate ligament reconstruction. Am J Sports Med 1993;21:338-342.
4. Harner CD, Irrgang JJ, Paul J, Dearwater S, Fu FH: Loss of motion after anterior cruciate ligament reconstruction. Am J Sports Med 1992;20:499-506.
5. Border WA, Noble NA: Transforming growth factor-beta in tissue fibrosis. N Engl J Med 1994;331:1286-1292.
6. Magit D; Wolff A; Sutton K; Medvecky M. Arthrofibrosis of the Knee. J Am Acad Orthop Surg 2007;15:682-694.
7. Fisher SE, Shelbourne KD (1993). "Arthroscopic treatment of symptomatic extension block complicating anterior cruciate ligament reconstruction". The American Journal of Sports Medicine. 1993; 21 (4): 558–64.
8. Shelbourne KD, Patel DV, Martini DJ. Classification and management of arthrofibrosis of the knee after anterior cruciate ligament reconstruction. Am J Sports Med. 1996 Nov-Dec;24(6):857-62.
9. Del Pizzo W, Fox JM, Friedman MJ, et al. Operative arthroscopy for the treatment of arthrofibrosis of the knee. Contemporary Orthopaedics 1985;10:67-72. 
10. Paulos LE, Wnorowski DC, Greenwald AE: Infrapatellar contracture syndrome: Diagnosis, treatment, and long term followup. Am J Sports Med 1994;22:440-449.
11. DeHaven KE, Cosgarea AJ, Sebastianelli WJ. Arthrofibrosis of the knee following ligament surgery. Instr Course Lect. 2003;52:369–381.
12. Laubenthal KN, Smidt GL, Kettelkamp DB. A quantitative analysis of knee motion during activities of daily living. Phys Ther. 1972;52: 34–43.
13. Perry J, Antonelli D, Ford W. Analysis of knee-joint forces during flexed-knee stance. J Bone Joint Surg Am. 1975;57: 961–967.
14. Cosgarea AJ, Sebastianelli WJ, DeHaven KE. Prevention of arthrofibrosis after anterior cruciate ligament reconstruction using the central third patellar tendon autograft. Am J Sports Med. 1995; 23:87–92.
15. Shapiro MS, Freedman EL. Allograft reconstruction of the anterior cruciate and posterior cruciate ligaments after traumatic knee dislocation. Am J Sports Med. 1995;23:580–587.
16. Noyes FR, Berrios-Torres S, BarberWestin SD, Heckmann TP: Prevention of permanent arthrofibrosis after anterior cruciate ligament reconstruction alone or combined with associated procedures: A prospective study in 443 knees. Knee Surg Sports Traumatol Arthrosc 2000;8:196-206.
17. Delay BS, Smolinski RJ, Wind WM, Bowman DS: Current practices and opinions in ACL reconstruction and rehabilitation: Results of a survey of the American Orthopaedic Society for Sports Medicine. Am J Knee Surg. 2001;14:85-91.
18. Melegati G, Tornese D, Bandi M, Volpi P, Schonhuber H, Denti M: The role of the rehabilitation brace in restoring knee extension after anterior cruciate ligament reconstruction: A prospective controlled study. Knee Surg Sports Traumatol Arthrosc 2003;11: 322-326.
19. Mikkelsen C, Cerulli G, Lorenzini M,Bergstrand G, Werner S: Can a postoperative brace in slight hyperextension prevent extension deficit after anterior cruciate ligament reconstruction? A prospective randomised study. Knee Surg Sports Traumatol Arthrosc 2003;11:318-321.
20. Dodds JA, Keene JS, Graf BK, Lange RH: Results of knee manipulations after anterior cruciate ligament reconstructions. Am J Sports Med 1991;19:283-287.
21. Kalson NS, Borthwick LA, Mann DA, Deehan DJ, Lewis P, Mann C, Mont MA, Morgan-Jones R, Oussedik S, Williams FM, Toms A, Argenson JN, Bellemans J, Bhave A, Furnes O, Gollwitzer H, Haddad FS, Hofmann S, Krenn V. International consensus on the definition and classification of fibrosis of the knee joint. Bone Joint J. 2016 Nov;98-B(11):1479-1488.
22. Aglietti P, Buzzi R, De Felice R, Paolini G, Zaccherotti G. Results of surgical treatment of arthrofibrosis after ACL reconstruction. Knee Surg, Sports Traumatol, Arthroscopy. 1995; 3:83-88.
23. Cosgarea AJ, DeHaven KE, Lovelock JE. The surgical treatment of arthrofibrosis of the knee. Am J Sports Med. 1994 Mar-Apr; 22(2):184-91.
24. Fisher SE, Shelbourne KD. Arthroscopic treatment of symptomatic extension block complicating anterior cruciate ligament reconstruction. Am J Sports Med. 1993 Jul-Aug;21(4):558-64.
25. Klein W, Shah N, Gassen A. Arthroscopic management of postoperative arthrofibrosis of the knee joint: indication, technique, and results. Arthroscopy. 1994 Dec;10(6):591-7.
26. Millett PJ, Williams RJ III, Wickiewicz TL: Open debridement and soft tissue release as a salvage procedure for the severely arthrofibrotic knee. Am J Sports Med. 1999; 27: 552–561.
27. Lobenhoffer HP, Bosch U, Gerich TG: Role of posterior capsulotomy for the treatment of extension deficits of the knee. Knee Surg Sports Traumatol Arthrosc. 1996; 4: 237–241.
28. Tardy N, Thaunat M, Sonnery-Cottet B, Murphy C, Chambat P, Fayard JM. Extension deficit after ACL reconstruction: Is open posterior release a safe and efficient procedure? Knee. 2016 Jun;23(3):465-71.
29. Wierer G, Runer A, Gföller P, Fink C, Hoser C. Extension deficit after anterior cruciate ligament reconstruction: Is arthroscopic posterior release a safe and effective procedure? Knee. 2017 Jan; 24(1):49-54 

Art of Creative Thinking

                     Art of Creative Thinking

                                 

                                           Dr KS Dhillon

What is creative thinking?

‘To create is always to do something new’.
                                                                   Martin Luther

“Creative thinking is not a talent, it is a skill that can be learnt.
It empowers people by adding strength to their natural abilities
which improves teamwork, productivity and where appropriate
profits”
                                                                                 Edward de Bono

The word creativity originated from the Latin term creō, which means to create or to make. It refers to the ability to generate new ideas and find original and useful solutions to problems [1]. 
Creative thinking is often referred to as, ‘thinking out of the box’, ‘lateral thinking’, or ‘divergent thinking’. In simple terms, it means looking at something in a new way. It is the ability to think differently and to perceive patterns that are not obvious. Creative thinking makes a person see things from a new angle or perspective.

Creative thinking allows a person to explore connections, meet new challenges and seek original, fresh and unusual solutions.

What is the need for creative thinking? 

Creative thinking has many advantages. Creative thinking helps a person to become a more confident, stronger, self-reliant and happier person. Creative thinking adds value not only to one’s life but also the life of others around. Open-minded thinking helps a person to explore new thoughts and ideas. Hidden talents surface, which allows a person to discover new opportunities, when creative thinking is adopted. There is no dead-end road for creative thinkers. There are endless opportunities to explore new challenges. Creative thinking gives a person a reason to wake up every morning and see what others cannot see.

The experiences gained through creative thinking makes it easier to handle difficult and challenging situations that come around. Creative thinking also makes a person happier and liked by people around.

How to enhance creative thinking skills?

Some believe that creative thinking techniques are based on experience. In 1996 this is what Steve Jobs had to say about creative thinking.

“Creativity is just connecting things. When you ask creative people how they did something, they feel a little guilty because they didn’t really do it, they just saw something. It seemed obvious to them after a while. That’s because they were able to connect experiences they’ve had and synthesize new things. And the reason they were able to do that was that they’ve had more experiences or they have thought more about their experiences than other people. Unfortunately, that’s too rare a commodity. A lot of people in our industry haven’t had very diverse experiences. So they don’t have enough dots to connect, and they end up with very linear solutions without a broad perspective on the problem”.

There are several ways in which creative thinking skills can be enhanced.

1.Counterfactual thinking

The term counterfactual literally means contrary to the facts. Counterfactual thinking is creating possible alternatives to life events that have already occurred which in fact is contrary to what actually happened. In counterfactual thinking thoughts such as ‘what if’ and ‘if I had only done that’ run through a person’s mind and the person wonders how things could have turned out differently. Counterfactual thoughts include things that could never happen in reality because they pertain to events that have occurred in the past.

A counterfactual thought occurs when a person alters a factual prior event and then goes on to assess the consequences of that change. A person imagines how the outcome could have been different if the antecedents which led to the event were different. For example, a nurse whose patient died while undergoing treatment in the ward may reflect upon how things could have turned out differently by imagining how some of the factors could have been different for a different outcome. The person would think that if she had given closer attention to the patient’s medical condition the patient may not have died.

There are two components in counterfactual thinking. The first is the activation portion and the second is content. The activation portion is when we allow the counterfactual thought to enter into our conscious thought and the content portion creates the end scenario for the thought that has entered the conscious[2].

Counterfactual thinking has both positive and negative consequences for the individual but the net result is an overall benefit for the individual.

Why do we allow ourselves to think of alternatives that can be beneficial or harmful to us? Many believe that humans tend to think of such counterfactual ideas in the presence of exceptional circumstances that led to an event which could have been avoided in the first place. Another reason why we use counterfactual thoughts is because we are close to an alternative outcome with positive outcomes [2].

Counterfactual thinking has a preparative function that helps people avoid past blunders and it makes a person feel better[3]. Counterfactual thinking is known to boost creativity for short periods of time.

2.Discovery-oriented behavior

According to Wertheimer [4], the function of thinking is not just to solve actual problems but to discover, envisage and go into deeper questions. In most great discoveries a certain question is often found. Envisaging and putting forward a productive question is a greater achievement than the solution of a question that has been set.

Research shows that real-world problem finding measure is predictive of creative thinking and real-world problem-finding measure is the most valuable predictor of creative potential [5].
Real-world problem finding is useful in enhancing creative thinking. For example, the nursing manager in the hospital ward can ask the nursing staff to think of as many different problems as possible, in their ward and come up with as many solutions as possible.

Creative thinkers don’t sit back and think of cut-and-dry end goals, they instead examine the problem from different angles before beginning to do the work.

3.Interpersonal distance and creativity

When there is a creative block, abstaining from a task is known to be useful. Now there is evidence which shows that creating “psychological” distance is also useful.

Jia et al [6] studied the effect of spatial distance on creative cognition and insight problem-solving. They were able to show that when a creative task is portrayed as originating from afar rather than a close location, individuals were able to provide more creative responses as well as perform better on problem-solving tasks that required creative insight. Individuals in their study were able to solve twice as many insight problems when they were asked to think about the source of the task which is distant, rather than closeby.

Förster et al [7] carried out six studies to investigate how and whether distant future time perspective promotes abstract thinking and at the same time impedes concrete thinking, by altering the level at which an individual’s mental representations are construed. They found that individuals who imagined themselves engaging in tasks a year later as compared to the next day performed better on a series of insight tasks. They also found that a distant perspective improved the creative generation of abstract solutions.

According to construal level theory (CLT), the distance of an individual from objects and events determines how abstractly the individual will represent or construe the objects and events. Whether events or objects are construed at lower or higher levels of abstraction would depend on conceptual differences as well as perceptual differences [8].

The contents of more abstract, higher-level construals consists of a summary of the given information about objects and events, whereas the content of lower-level construals consists of contextual and readily observable features [8]. Higher-level construals involve broad and global processing of information whereas lower-level construals involve narrow and localized processing of information[8]. The main tenet of CLT is that increasing the distance of an individual from objects and events is associated with more abstract construals. Creativity increases as the spatial distance increases.

One has to try to imagine that one’s creative task is disconnected and distant from one’s current position or location. This will make the problem more accessible and it can encourage higher-level thinking.

4.Embracing absurdity

Research shows that reading and or experiencing something unreal or absurd can boost pattern recognition and creative thinking. The mind is always trying to make sense of the things that a person sees. Absurd and unreal things put the mind in overdrive for short periods of time while the mind works out what it is looking for [9].

Proulx and Heine [9] were able to show that novel patterns of association learning could be enhanced by unrelated meaning threats. They found that the ‘cognitive mechanisms responsible for implicitly learning patterns are enhanced by the presence of a meaning threat’ [9]. Meaning threats whatever their source motivate people to seek out meaning somewhere else. Meaning threats can be to an individual’s self-esteem, threats to their political worldview, threats to their sense of situational certainty, threats to their existence or threats to their goal attainment [9].

Reading interesting absurd short stories and seeing absurd art can provide inspiration to individuals.

5. Let your mind wander

There is a link between mind-wandering and crucial parts of our daily lives, including affect, learning and job productivity. Mind-wandering is limited in the morning and it increases throughout the morning and peaks at midday. It decreases through the afternoon and peaks again in the evening [10].
A wandering mind can boost creative thinking. It allows you to access new ways of processing and imagining and help you to come up with new solutions to old problems. It can inspire an individual to write new stuff and learn new languages. It is a creative minds’ ultimate asset.

A wandering mind encourages inquisitiveness which in turn increases the desire for information and knowledge. It also stretches one's imagination and lays the fountain for creativity. The newfound creativity opens up new avenues of thinking, planning, preparing and ultimately doing things.
Self-imagination and awareness of self increases when the mind wanders.

Self-imagination allows the transfer of short term memory to long term memory by concentrating on the meaning of the information. Self-imagination helps with retrieval of memory and it also brings about a sense of self.

6. Day time naps and sleep

A nap of between 10 min to 30 min duration during the day is known to promote wakefulness and enhance performance and improve learning ability. Longer naps, on the other hand, are associated with a loss of productivity and sleep inertia. The habit of taking frequent and long naps especially among the elderly may be associated with higher morbidity and mortality [11].

Nocturnal sleep provides pivotal insights. Insight is mental restructuring which leads to a gain of knowledge which brings about qualitatively changed behavior. Sleep allows the consolidation of recent memories.

A study by Wagner et al [12] showed that sleep, by restructuring new memory and representations, facilitates extraction of explicit knowledge and insightful behaviour.

7. Conceptualize the problem in a new way

Creative people generally look at problems in a new way more often as compared to less creative people. Creative people avoid cut-and-dry end goals and they examine the problem from different angles before starting on a job. Creative individuals focus on fundamental parts of the problem and they look at a more meaningful angle of the problem which leads them to something that is original.

8. Embrace your limitations

Many believe that freedom gives you the space to be a better creator. This is not true because history shows us that most creative endeavors took place within limited environments with restricted budgets and individuals who had an abundance of talent and finances often fail to create anything original.
It is well known that creativity is not born from freedom. We have to push ourselves beyond our limits to learn a skill, absorb the rules, learn where the limits are and try to exceed them. Staying inside a box helps us think outside it by looking at light shining through the cracks in the box.
Imposing restrictions or limitations can actually boost creativity, which is the ultimate defense against a creative block. More freedom can be crippling. When we have more options than it is harder to make decisions. When we add limitations to our creative process it helps us to stay motivated and we find new ways to handle the difficulty.

Limitations challenge the way we think and it forces us to think in new ways. Creative problem solving keeps our mind sharp. Thinking of limitations makes our brain work harder and peculiar limitations push the mind to work harder.

Limitations yield more interesting results and it leads us down new paths which we may be unfamiliar with. One must avoid taking the path of least resistance and building on ideas that we already have and using all the resources available. We need to impose limitations which can boost our creativity and force us to work outside of our comfort zone.

8. Mood and creativity

“Feeling and longing are the motive forces behind all human endeavour and human creations”
                                    Albert Einstein, Religion and Science

Creativity is critical for both survival and prosperity. Hence people adapt to changing environment by generating new insights and solving problems. One of the most studied predictors of creativity is mood.

Baas et al [13] carried out a meta-analysis of 25 years of mood-creativity research. They found that positive moods produce more creativity than mood-neutral controls and there were no significant differences between negative moods and mood-neutral controls.

Moods with positive hedonic tone (e.g happiness and relaxed state) bring about greater creative performance as compared to moods with negative hedonic tone (e.g fear and sadness) or neutral mood control conditions. The reason for this is that positive hedonic tone increases cognitive flexibility and inclusiveness. Negative activating moods such as fear and anxiety are associated with lower creativity.

Moods with positive hedonic tones are associated with an increase in dopamine levels in the anterior cingulate cortex of the brain. Dopamine mediates many of the cognitive effects of positive affect. Increased levels of dopamine promote creative thinking.

Some investigators have found the opposite effect of mood on creativity. Kaufmann et al [14] in a study found that positive mood led to significantly poorer creative problem-solving performance and negative mood significantly facilitated creative problem-solving relative to induced neutral mood. They found that the poorest performance was obtained in the positive mood condition.
Overall most studies show that a positive mood is associated with creativity.

9. Exercise and creativity

There is a link between physical exercise and favorable moods and this has been well established. Various kinds of exercise such as aerobic workout, jogging, running, cycling as well as treadmill have been shown to enhance mood [15]. Steinberg et al [15] carried out a study to assess if exercise enhances creativity independently of mood. They found that mood was significantly improved by aerobic exercise as compared with a neutral video control group. They also found that there was a consistent increase in creativity with exercise. They concluded that creativity and mood improved with physical exercise independently of each other.

10. Pursue weird or different experiences

“Creativity comes from looking for the unexpected and stepping outside your own experience.” ~Masaru Ibuka

It is well known that creative people can be eccentric. History shows us that many poets and playwrights had odd behavior and this has been observed by well-known people like Plato and Aristotle. History tells us that Albert Einstein used to pick up cigarette butts from the street to get tobacco for his pipe. Howard Hughes used to spend full days on a chair in the middle of his Beverly Hills Hotel suite because he believed that the suite was germ-free. The famous German composer and critic, “Robert Schumann believed that his musical compositions were dictated to him by Beethoven and other deceased luminaries from their tombs and Charles Dickens is said to have fended off imaginary urchins with his umbrella as he walked the streets of London” [16].

Research has established that there is a connection between creativity and eccentricity. This association is often seen in individuals with schizotypal personality which is a milder version of schizotypal personality disorder.

According to Shelley Carson [18], schizotypal personality can appear in a variety of forms, some of which include magical thinking, unusual perceptual experiences, social anhedonia, and mild paranoia.

There are several studies which show that creative people tend to score higher on schizotypal surveys. Carson also found that some creative students report “magical thinking and odd perceptual experiences” such as hearing whispering voices in the wind. [18].

Schizotypal personality does not predispose an individual to creativity.  Cognitive disinhibition appears to be the underlying factor in eccentricity. Cognitive disinhibition occurs when an individual is unable to ignore irrelevant or immaterial information.

There is a large amount of data that we are bombarded with throughout the day and it is not possible to attend to all this data on a daily basis. To prevent this data from reaching our conscious awareness we all possess mental filters. One of these filters is called latent inhibition (LI). LI has been
defined by Carson and colleagues as: “the varying capacity of the brain to screen from current attentional focus stimuli previously experienced as irrelevant”[17]. Research shows that reduced LI is associated with increased vulnerability to schizophrenia. Low LI has also been found to contribute to original thinking especially in combination with high IQ.

It is well known that not everyone who’s weird is creative. This is because research shows that only individuals with low LI who have high IQ are creative [17].

Highly creative individuals and psychotic-prone individuals probably possess neurobiological similarities which are genetically determined and they present either as psychotic predisposition or as unusual creative potential.

11. Challenge your brain. 

Problem-solving is the key to creativity. The commonly used approach to creative problem solving (CPS) is the 6-diamond model [18].

The 6 steps include [19]:

•  Mess finding: The areas of concern are identified. Ideas are generated for possible solutions. Three most critical problems are identified and one is selected for further work.
•  Fact-finding: Careful observation is necessary while collecting information  about the problem situation. Both objective and subjective information is collected, identified and explored. 
•  Problem finding: Look at the problem from different angles and think of other possibilities.
•  Idea Finding: Look for a variety of ideas, alternatives, options, approaches, paths, methods and tools to select potential ideas or solutions.
• Solution finding: Look at all the ideas in new and different ways. Consider the consequences, implications, and reactions to the ideas selected. Once the ideas have been selected and solutions found than develop an action plan.
•  Acceptance finding: Once the action plan has been developed, think of ways to implement the action plan. Ways must be found to make the ideas and solutions more attractive, more effective, more acceptable and more beneficial. Working plan for implementation must be developed.

There has been a lot of research into the CPS process which shows that there is a need for willingness to consider alternatives, to take risks, to venture into insecure areas and to tolerate some uncertainty and ambiguity [20].

12. Chart your own path.

“Act! Action will delineate and define you.”
                                     Thomas Jefferson.

It is well known that the only person who can promote yourself is you. There is no one who will promote you or put you in the limelight unless you do it yourself. You have to sell your story yourself.

Well known people who charted their own path include Steve Job, Bill Gates, Thomas Eddison, Wright brothers, James Watt and the list goes on and on.

Only we ourselves can define and determine our destiny. We have the responsibility of managing our thoughts. Positive thinking will spur us to positive actions and productive habits. Good habits will shape a positive fruitful future.

We have to stay away from defeatist, discouraging and disillusionary thoughts and negative attitude. We have to stay away from people who belittle our dreams. You are the best person to set your own goals.

Charting our own creative path helps us open doors which we might have never known existed. Trailblazers are people who hold hands with fear and they are willing to risk venturing into the unknown rather than staying in familiar surroundings. They are willing to venture into the unknown
Nobody can discover the world for us, we have to discover it ourselves.

Conclusion

Creative thinking refers to one’s ability to generate new ideas and find original and useful solutions to problems. Sometimes it is referred to as, ‘thinking out of the box’, ‘lateral thinking’, or ‘divergent thinking’. It is the ability to think differently and to perceive patterns that are not obvious. It makes a person see things from a new angle or perspective and it allows a person to explore connections, meet new challenges and seek original, fresh and unusual solutions.

Creative thinking helps a person to become a more confident, stronger, self-reliant and happier person. Creative thinking adds value not only to one’s life but also the life of others around.
There are several ways in which creative thinking can be enhanced and these are explored in some detail in this article.

References

1. Ritter, S. M. & Mostert, N. Enhancement of Creative Thinking Skills Using a Cognitive-Based Creativity Training. J Cogn Enhanc. 2017; 1, 243–253.
2. Roese N. Counterfactual thinking. Psychological Bulletin. 1997; 121 (1): 133–148.
3. Olson JM & Roese N J. Relative deprivation and counterfactual thinking. In Walker, I. and Smith, H. J. (Eds.). Relative deprivation: Specification, development, and integration. 2002. pp.  265–287. Cambridge, UK: Cambridge University Press.
4. Wertheimer, M. Productive thinking.1945 New York: Harper & Row.
5. Okuda SM, Runco MA, Berger E. Creativity and the finding and solving real-world problems. J of Psychoeducational assessment. 1991; 9: 45-53.
6. Jia L, Edward R, Hirt, Karpen SC. Lessons from a Faraway land: The effect of spatial distance on creative cognition. Journal of Experimental Social Psychology. 2009; 45(5):1127-1131
7. Förster J, Friedman RS, & Liberman N. Temporal Construal Effects on Abstract and Concrete Thinking: Consequences for Insight and Creative Cognition. Journal of Personality and Social Psychology. 2004; 87(2), 177-189.
8. Henderson MD, Wakslak CJ, Fujita K and Rohrbach J. Construal Level Theory and Spatial Distance Implications for Mental Representation, Judgment, and Behavior. Social Psychology 2011; Vol. 42(3):165–173.
9. Proulx T, Heine SJ. Connections from Kafka: exposure to meaning threats improves implicit learning of an artificial grammar. Psychol Sci. 2009 Sep;20(9):1125-31.
10. Smith, Gabriel King, et al. “Mind-wandering rates fluctuate across the day: evidence from an experience-sampling study.” Cognitive research: principles and implications. 2018; 3 (1): 54.
11. Dhand R, Sohal H. Good sleep, bad sleep! The role of daytime naps in healthy adults. Curr Opin Pulm Med. 2006 Nov;12(6):379-82.
12. Wagner U, Gais S, Haider H, Verleger R, Born J. Sleep inspires insight. Nature. 2004 Jan 22;427(6972):352-5.
13. Baas M, De Dreu CK, Nijstad BA. A meta-analysis of 25 years of mood-creativity research: hedonic tone, activation, or regulatory focus? Psychol Bull. 2008 Nov;134(6):779-806.
14. Kaufmann G and & Vosburg SK. (1997). Paradoxical mood effects on creative problem-solving. Cognition and Emotion. 1997; 11: 151-170.
15. Steinberg H,Sykes EA, Moss T,Lowery S,LeBoutillier N,Dewey A. Exercise enhances creativity independently of mood. Br J Sports Med.1997;31:240-245.
16. Shelley Carson. Your Creative Brain: Seven Steps to Maximize Imagination, Productivity, and Innovation in Your Life. 2010, Jossey-Bass publisher, Harvard University.
17. Carson SH, Peterson JB, Higgins DM. Decreased latent inhibition is associated with increased creative achievement in high-functioning individuals. J Pers Soc Psychol. 2003 Sep;85(3):499-506.
18. Courger J.D. (1995) Creative Problem Solving and Opportunity Finding. 1995 Boyd and Fraser publishing company.
19. Vidal R. Creativity for OperationalResearchers. Investigacao Operacional. 2005;25:1-24.
20. Parnes, S.J. (1997) Optimize the Magic of your Mind, NY: Bearly Limited.

Long Term Outcome of Treatment of Subaxial Cervical Spine Fractures

              Long Term Outcome of Treatment of Subaxial Cervical Spine Fractures

                                                          Dr KS Dhillon

Classification of subaxial cervical spine fractures

The widely used classification for lower cervical spine injuries is the one by the AO group. It divides lower cervical spine injuries into 3 types i.e type A, B, C based on the trauma mechanism.

A: compression
B: distraction
C: rotation

Type A compression injuries are further subdivided into type:
 A.1  =  impaction
 A.2  =  split
 A.3  =  burst.

Type B distraction injuries are further subdivided into:
 B.1  =  posterior distraction with vertebral body intact
 B.2  =  posterior distraction + fracture of the vertebral body
 B.3  =  anterior distraction + hyperextension.

Type C rotation injuries are subdivided into:
C.1  =  unilateral facet fracture-dislocation
C.2  =  unilateral facet dislocation
C.3  =  rotational shear injury of the joint mass.

To remedy a lack of consensus on the classification of lower cervical spine injuries the Subaxial Injury Classification (SLIC) Scale was created [1]. This classification takes into account morphology; status of the disco-ligamentous complex and neurological assessment.



Table 1. Subaxial Injury Classification (SLIC) scale.
   
Morphology                                                                                                  Points
No abnormality                                                                                               0
Compression + burst                                                                                1 + 1  =  2
Distraction (e.g., facet perch or hyperextension)                                            3
Rotation or translation (e.g., facet dislocation, unstable teardrop,
or advanced-stage flexion-compression injury)                                              4

Disc-ligamentous complex
Intact                                                                                                               0
Indeterminate (e.g., isolated interspinous widening or MRI signal
change only)                                                                                                    1
Disrupted (e.g., widening of the anterior disk space or facet perch
or dislocation)                                                                                                  2

Neurological status
Intact                                                                                                              0
Root injury                                                                                                      1
Complete cord injury                                                                                      2
Incomplete cord injury                                                                                    3
Continuous cord compression (neuro-modifier in the setting of a
neurological deficit)                                                                                     + 1

Based on the above parameters, scores are assigned to each injury. Patients with a score lower than 4 will need nonsurgical treatment and patients with scores higher than 4 will require surgical treatment. Patients with a score of 4 can be treated surgically or nonsurgically depending on the experience of the surgeon.

Treatment of subaxial cervical spine fractures

Unfortunately, there is insufficient evidence to recommend treatment standards and there is also insufficient evidence to recommend treatment guidelines for subaxial cervical spine injuries [2]. The main principles of treatment include decompression of compressed neurological structures, restoration of vertebral column integrity, prevention and management of complications, and facilitation of rehabilitation [3].

Subaxial Injury Classification (SLIC) Scale has been introduced to help in decision making for treatment of subaxial injuries [1]. Generally, patients with a score lower than 4 are treated nonsurgically while patients with scores higher than 4 are treated with surgery. Patients with a score of 4 can be treated surgically or nonsurgically depending on the experience of the surgeon.
Many patients with cervical spine injuries can be treated nonoperatively. Options for conservative treatment include the use of a cervical orthosis or rigid stabilization with a halo jacket.

In patients with displaced cervical spine injury, a closed reduction can be carried out. It is safe to treat displaced subaxial fracture and subaxial subluxations and dislocations, by traction [3].

Lee et al [4] carried out a study involving 210 patients with unilateral and bilateral facet dislocations. They found that rapid traction under sedation using weights up to 150 pounds was safer than carrying out manipulation under anesthesia. They also found that early reduction of the dislocation in patients with neurological deficit gave them the best chance of neurological recovery.

Surgery is usually indicated in patients when a close reduction has failed, in patients with unstable injuries and when there is bilateral facet dislocation of more than 25% or 11°. Progressive neurological deterioration would be another indication for surgery. Kyphosis of 30° or more or loss of vertebral height of more than 50% is often associated with a high incidence of late complications, and this situation may warrant surgical intervention. Late instability and severe post-traumatic kyphosis may warrant surgical intervention [3].

In patients with partial neurological injury, early surgical intervention is usually recommended. There is some evidence that early surgical intervention (less than 24 hours) is safe and effective. Neurological recovery can also occur in some patients who have delayed decompression [4,5].
Some have claimed that 70% of patients with partial spinal cord injury improve one grade or more (American Spinal Injuries Association, International Medical Society of Paraplegia grades) if the surgery is carried within 6 hours after the injury [7]. When surgery is carried out after 6 hours only 12% of the patients show improvement. In patients with a complete spinal cord injury, the chances of neurological recovery is poor.

Decompression and/or stabilized of the cervical spine can be carried out via the anterior, posterior or a combination of both approaches, depending on the type of injury. The clinical success rates are higher with the anterior approach through the anterior approach is biomechanically inferior to the posterior approach [3].

Long term outcome of cervical spine injury treatment

There is a dearth of literature on the long term outcome of management of cervical spine injuries. The largest study with a long term follow up is the one by Fredø et al [8]. They followed up 256 patients with subaxial cervical spine injuries who were treated surgically. The surgical approach was anterior in 69% of the patients, posterior in 22% and combined in 9 % of the patients.
The mean follow-up period was 3.1 years with a range of 0.5–9.0 years. None of their patients had neurological deterioration after the surgery.

In patients who were operated within 24 hours, 48.8% showed improvement of their neurological grades, whereas in patients operated after 24 hours 53.1% showed improvement in their neurological grades. The improvement in AIS (American Spinal Injury Association impairment scale) grades between the two groups were not significantly different (p = 0.442). Of the patients with preoperative radiculopathy, 11 % of the patients continued to have radicular symptoms. There were four patients who developed radiculopathy after surgery, three of these patients were asymptomatic at follow-up.
Neck pain was assessed using the Visual Analog Scale (VAS). They found that the median VAS score for neck pain was 1 (range 0–10). Eighty percent of the patients had VAS scores ≤3, 15 % had VAS scores 4–6, and 5 % had VAS scores ≥7. There was no significant association between the surgical approach and neck pain [8].

They found that 26% of the patients had no neck stiffness, 63% had mild neck stiffness and 11% had severe neck stiffness. Neck stiffness was more common in patients who had fusion with posterior screw fixation.

Six percent of patients sustained hoarseness and 9% developed dysphagia after surgery. Of the 256 patients who were followed up with cervical CT scans, 98.4 % had a stable fusion, 0.4 % had a secondary loss of alignment, and in 1.2 % of the patients, there was loosening or fracture of their fixation device[8]. In this study, the surgical mortality(death within 30 days after surgery) was 2.3 %.
Koller et al. [9] carried out a retrospective review of 28 patients who had anterior cervical decompression, fusion, and plating (ACDFP) for unstable subaxial injuries without neurological deficit, to assess the mid- to long-term outcome. The mean follow up period was 5.5 years (range16–128 months). The self-rated clinical outcome was excellent or good in 81% of patients and moderate or poor in 19% of the patients.

Construct failure was seen in 31% of cases.  The fusion rate was 88.5%.  Adjacent-level degeneration progression was significantly influenced by a decreased plate-to-disc-distance. The motion of adjacent level intervertebral space was not altered due to the adjacent fusion, but it was reduced in the presence of advanced adjacent level degeneration.

Conclusion

There is a dearth of literature on the long term outcome of management of cervical spine injuries. The largest study with a long term follow up is the one by Fredø et al [8]. They followed up 256 patients with subaxial cervical spine injuries who were treated surgically. The mean follow-up period was 3.1 years with a range of 0.5–9.0 years. They obtained stable fusion in 98.4% of the patients, 0.4 % had a secondary loss of alignment, and in 1.2 % of the patients, there was implant failure. The surgical mortality (death within 30 days after surgery) was 2.3 %.

Koller et al. [9] carried out a small retrospective review of 28 patients who had anterior cervical decompression, fusion, and plating (ACDFP) for unstable subaxial injuries without neurological deficit, to assess the mid- to long-term outcome. The mean follow up period was 5.5 years (range16–128 months). Their results were not as good as the ones reported by Fredø et al [8]. Construct failure rates were very high with an incidence of 31%. Their fusion rates were lower at 88.5%.

To date, no other studies on the long term outcome of management of subaxial cervical spine injuries, have been published.

References

1. Dvorak MF, Fisher CG, Fehlings MG, Rampersaud YR, Oner FC, Aarabi B, et al. The surgical approach to subaxial cervical spine injuries: an evidence-based algorithm based on the SLIC classification system. Spine (Phila Pa 1976) 2007;32(23):2620–9.
2. Hadley MN, Walters BC, Grabb PA, Oyesiku NM, Przybylski GJ, Resnick DK, Ryken TC. Treatment of subaxial cervical spinal injuries. Neurosurgery. 2002 Mar;50(3 Suppl): S156-65.
3. O'Dowd JK. Basic principles of management for cervical spine trauma. Eur Spine J. 2010 Mar; 19(Suppl 1): 18–22.
4. Lee AS, MacLean JC, Newton DA. Rapid traction for reduction of cervical spine dislocations. J Bone Joint Surg Br. 1994 May;76(3):352-6.
5. La Rosa G, Conti A, Cardali S, Cacciola F, Tomasello F. Does early decompression improve neurological outcome of spinal cord injured patients? Appraisal of the literature using a meta-analytical approach. Spinal Cord 2004;42:503-12.
6. Fehlings MG, Perrin RG. The role and timing of early decompression for cervical spinal cord injury: Update with a review of recent clinical evidence. Injury 2005;36 Suppl 2:B13-26.
7. Fehlings M, Aarabi B, Dvorak M, et al. (2008) A prospective multicenter trial to evaluate the role and timing of decompression in patients with cervical spinal cord injury: initial one-year results of the STASCIS study. Paper presented at the AANS meeting in Chicago.
8. Fredø HL, Rizvi SAM, Rezai M, Rønning P, Lied B and Helseth E. Complications and long-term outcomes after open surgery for traumatic subaxial cervical spine fractures: a consecutive series of 303 patients. BMC Surg. 2016 Aug 15;16(1):56.
9. Koller H, Reynolds J, Zenner J, Forstner R, Hempfing A, Maislinger I, Kolb K, Tauber M, Resch H, Mayer M, Hitzl W. Mid- to long-term outcome of instrumented anterior cervical fusion for subaxial injuries. Eur Spine J. 2009 May;18(5):630-53.