Carpal Tunnel Syndrome--Revisited

                   Carpal Tunnel Syndrome--Revisited

                       

                                                    DR KS Dhillon

Chronic carpal tunnel syndrome was first described by James Jackson Putnam in 1880. Other medical luminaries have shed more light on the subject in the subsequent years including Paget, Marie, Ramsay Hunt, Phalen and Osler [1]. Carpal tunnel syndrome is probably the most common peripheral compression neuropathy and is defined by compression of the median nerve at wrist level.

Anatomy of the carpal tunnel

The carpal tunnel is a rigid non expendable osteofibrous tunnel situated on the front of the wrist. Anteriorly it is bound by the flexor retinaculum and posteriorly lies the carpal sulcus. Medially lies the hamate hook,triquetral bone and pisiform bone, and laterally lies the scaphoid bone, trapezoid bone and tendon of the flexor carpi radialis (FCR) muscle. The sulus is formed by the capsule, and the anterior radiocarpal ligaments which cover the proximal row of carpal bones.

Besides the median nerve there are four superficial and four deep flexor tendons of the fingers in the tunnel. On the radial side there is the long flexor of the thumb.
The location of the median nerve in relation to other structures changes as it traverses the tunnel. At the entrance the nerve lies deep to the palmaris or between the palmaris and the flexor carpi radialis.
In neutral wrist position, it usually lies anterior to the superficial flexor of the index or the middle finger with the long thumb flexor on the radial side.

More distally in the palm the nerve divides into six branches: the thenar motor branch; three specific palmar digital nerves to the radial and ulnar side of the thumb and radial side of the index finger and two common palmar digital nerves of the second and third web spaces.

Anatomical variations of the carpal tunnel structures

There are several anatomical variations in and around the carpal tunnel which affect the nerves, tendons and arteries. These variation are responsible for variation in the clinical presentation and may lead to intraoperative complication during surgery.

Some of the variations include the following [2]:

A. Nerve anomalies

• High bifurcation of median nerve (1% to 3.3% of patients undergoing surgery). The radial median branch may have its own tunnel.
• Aberrant origin of motor branch of median nerve. There can be 5 variation. Most often the branch arises distal to the carpal tunnel which is the norm. In about a third of the cases it arises within the canal and in about a quarter of the cases the branch pierces the transverse carpal ligament and courses to the thenar muscles. Rarely the branch arises on the ulna and anterior side of the median nerve and crosses anterior to the median nerve on its way to the thenar area. In some patients it enters the palm superficial to the transverse carpal ligament.
• Variations in path of palmar cutaneous branch of median nerve. Normally the palmar cutaneous branch arises proximal to the carpal tunnel and enters the palm superficial to the carpal ligament. There are two other variations, one where it pierces the carpal ligament on its way to the palm and second where it courses on the ulna side of the median nerve.
• Anomalous course of ulnar nerve. The ulnar nerve usually enters the palm through the Guyon’s canal, a depression between the pisiform bone and the hook of the hamate. Occasionally the ulnar nerve has been found to traverse the carpal tunnel and the patients can present with carpal tunnel syndrome associated with symptoms of ulnar nerve compression.
• Median nerve (MN) and ulnar nerve (UN) anomalous anastomoses. There are four commonly described anomalous connections between the MN and UN. The most common anomalous anastomosis is between the connection from MN to UN in the forearm which is known as the Martin Gruber anastomosis (MGA). The interneural connections from UN to the MN is known as the Marinacci anastomosis. When there is an interneural connection between common digital nerves of UN and MN nerves in the palm of the hand it is called the Barrettini anastomosis.  An anomalous connection from the UN to the MN in the hand is known as the Riche–Cannieu anastomosis where there is a crossover in the palm, between the deep branch of the UN and the recurrent branch of the MN. 

 B.Tendon anomalies

• Conjoint FPL and FDP II (Linburg-Comstock syndrome). In some individuals there is an anomalous tendinous connection between the FPL and the FDP tendons to the index and sometimes the middle finger. In such circumstance the individual is unable to flex the DIP joint of the thumb without concomitant flexion of the dip joint of the the finger. This can lead to tendonitis which can mimic symptoms of carpal tunnel syndrome.

C. Vascular anomalies

• Persistent median artery. A persistent median artery is sometimes seen traversing the carpal tunnel. It can significantly contribute to vascularity of the hand. Sometimes it is present with bifurcated median nerve. The presence of this artery does not produce any symptoms but may get severed during a carpal tunnel release.
• Superficial ulnar artery.The ulnar artery sometimes takes a superficial course within the forearm and travels superficial to the muscles but deep to the antebrachial fascia where it risks being severed during an extended carpal tunnel release.

D.Muscle anomalies

• Palmaris longus. The palmaris longus muscle is one of the most variable muscles in the human body. Two variations of palmaris longus are related to the anatomy of the carpal tunnel. In some individuals the tendon of the palmaris longus traverses the carpal tunnel and inserts into the palmar fascia distally. In other individuals the muscle belly of the palmaris longus may be situated in the carpal tunnel.
• Index lumbrical. The lumbrical muscle to the index finger may arise  proximally on the FDS within the carpal tunnel and can cause carpal tunnel compression syndrome.
• Flexor digitorum superficialis indicis. In some individuals the FDS muscle may be present in the carpal tunnel along the index finger tendon and cause carpal tunnel syndrome.

Etiology of carpal tunnel syndrome(CTS)

In most of the patients there is no known cause for the CTS and it is than referred to as idiopathic CTS. In some case it is due to factors around the canal or within the canal and than it is referred to as secondary CTS.

Idiopathic carpal tunnel syndrome

Idiopathic CTS is usually seen in females (65–80%), between the ages of 40 and 60 years. In about 50–60% of the patients it is bilateral [3]. Anthropometric factors such as size of the canal, sex, age and genetic factors are the most important predisposing factors. Repetitive manual
activities, exposure to vibrations, cold temperatures, obesity and smoking have also been implicated as predisposing factors for carpal tunnel syndrome [4,5].

Secondary carpal tunnel syndrome [6]

A. Abnormalities of the wall of the carpal tunnel

Conditions that alter the condition of the walls of the canal can cause compression of the median nerve. These include:

• Carpal bone subluxation or dislocation
• Distal radius fractures and implants used for fixation of fractures can reduce the carpal tunnel space
• Wrist joint arthritis, degenerative and inflammatory
• Acromegaly.   

 B. Abnormalities of content of the tunnel [6]

• Tenosynovial hypertrophy 
• Inflammatory tenosynovitis due to rheumatism, lupus and infection
• Metabolic tenosynovitis due to diabetes mellitus, amyloidosis, gout and chondrocalcinosis
• Abnormalities of fluid distribution due to pregnancy, hypothyroidism and chronic kidney failure  
• Intratunnel tumors such as lipoma, synovial cyst, synovial sarcoma, schwannoma, neurofibroma or lipofibroma
• Hematoma due to hemophilia, anticoagulant accident or trauma
• Obesity

Repetitive flexion and extension of the wrist, flexion of the fingers and forearm supination has been implicated in an increase of pressure within the canal which can predispose an individual to CTS. An increase in prevalence of CTS has been seen in individuals who work more than 20 hours per week on the computer [7]. Exposure to vibration causes injury of the myelin and axons leading to ultrastructural microcirculatory compression problems and intraneural edema which can sometimes produce CTS [8] .

Diagnosis of carpal tunnel syndrome

The typical symptoms are nocturnal acroparesthesias comprising of tingling, numbness, swelling or hypoesthesia, with or without pain reaching at least two of the first three fingers and the palm. Night pain is the most  sensitive symptom predictor (96%) in patients with CTS [9].

The Durkan's compression test [10] which is performed by compression of the median nerve in the carpal tunnel for as long as thirty seconds has a 89% sensitivity [9].

Semmes-Weinstein Monofilament Testing and Phalen's maneuver has a 83% sensitivity and hand diagram scores have a 76% [9] to 80% sensitivity [11]. The Tinel's sign has a 71% sensitivity. Some have found that the Tinel’s sign has no diagnostic value in patients with CTS [12].

Electroneuromyography (ENMG) examination

An ENMG examination is used to study the sensory and motor nerve conduction of the median nerve through the wrist. Analysis of the amplitude and duration of the sensory and motor responses is done.
Bilateral ulna and median nerve studies are carried out.

In CTS focal demyelination occurs, hence nerve conduction study (NCS) is usually more valuable than needle electromyography (EMG) study. Meticulous attention has to be paid to ‘electrode placement, distance measurements, stimulation intensity, skin temperature, and many others factors are important to prevent misdiagnosis of CTS’ [13]. The skin temperature should be maintained at about 32C for NCS.

Sensory Conduction Studies

In patients with mild or early CTS there is a mild sensory nerve conduction slowing across the carpal tunnel. A delayed or prolonged peak latency of the median sensory nerve action potential (SNAP) is typically seen.

The peak latency is usually used, instead of onset latency, for detecting CTS because of difficulty in identifying the onset of the SNAP in the presence of a large stimulus artifact [13]. With progress of the CTS the  sensory peak latency gets further delayed with the amplitude becoming smaller. In severe CTS, there usually is no recordable SNAP despite signal averaging and enhancement.
The most commonly used protocol (antidromic technique), for median nerve sensory conduction study, is the one where stimulation is applied at the wrist and median SNAPs are recorded at the thumb, the index, the middle and ring fingers [13].

Motor Conduction Studies

Motor nerve conduction of the median nerve is usually measured by obtaining recordings over the abductor pollicis brevis (APB) muscle. A delay of the distal motor latency (DML) usually supports the diagnosis of CTS. A mild prolongation of the median DML, however does not suggest focal demyelination of the median nerve [13].

Sensitivity of electroneuromyography (ENMG) examination

ENMG examination may be positive in 0–46% of asymptomatic subjects and negative in 16–24% of patients with a clinical diagnosis of CTS [14,15,16,17].

The sensitivity of motor distal latency in the diagnosis of CTS is about 54% [18]. ENMG examination does not provide extra evidence in diagnosis of CTS when the clinical diagnosis is obvious [19]. Anatomical variations such as the Martin–Gruber and Riche–Cannieu types can affect the interpretation of the ENMG examination.

Treatment of carpal tunnel syndrome

Conservative Treatment

In patients with medical causes for CTS, the underlying medical condition is treated such as ‘diuretics for fluid retention, thyroid supplementation for hypothyroidism, insulin for diabetes, and immune modulating agents for rheumatoid arthritis’ [13].

Nighttime splinting of the wrist in neutral position has been found to be useful in reducing nocturnal symptoms. Oral anti-inflammatory drugs do reduce synovitis and provide relief in some patients. The use of pyridoxine (vitamin B6) for treatment of CTS has been abandoned since it has been found to be of no value in the treatment of patients with CTS.

Though prospective studies [20,21] have shown effectiveness of the use of local steroid injections in the treatment of CTS, a Cochrane database  systematic review by Marshall et al [22] showed that local corticosteroid injection for carpal tunnel syndrome provides greater clinical improvement in symptoms for only one month after injection compared to placebo. They found that there was no significant symptom relief beyond one month. The clinical outcome was no better with steroid injection as compared to NSAIDs and splinting after 8 weeks. Steroid injections should probably not be used as an option in the treatment of CTS.

Patient education is useful in patients with work related CTS where they are advised to avoid activities which aggravate the symptoms and to do simple hand and wrist exercises. Evaluation of the workstation and redesigning the workstation along with ergonomic tool modification is often useful in work related CTS [9].

Surgical treatment for carpal tunnel syndrome

In patients with acute CTS due to trauma from fractures and dislocations around the wrist and due to bleeding, immediate surgical intervention to relieve the pressure on the nerve is usually mandatory.
In patients with subacute and chronic CTS where conservative treatment has not helped and in patients with moderate to severe symptoms, surgical release of the carpal tunnel is known to be effective [23].

Carpal tunnel release or carpal tunnel decompression surgery involves the division of the flexor retinaculum/transverse carpal ligament by open or endoscopic surgery. The existing literature shows that the long term outcome of open carpal tunnel release (OCTR) is generally good. There are wide variations in success and failure rates reported in literature, partly due to variations in patient selection and variations in the definition of success and failure. Clinical success has been reported in 75–90 % of the patients and recurrence rates of between 4–57 % have been reported [24].
The long term outcome with endoscopic surgery is indistinguishable from that of open carpal release. There are a small number of studies which suggest that there is a higher incidence of recurrence with techniques other than OCTR [24].

There is only one study by Pensy et al [25] which asserts that the functional outcome of surgical treatment is not significantly different from that of conservative treatment on long-term follow-up, though the improvement in symptom scores was greater in surgical patients.
Literature review shows that ENMG examination, the only objective data available, tends to suggest that there are long-term, persistent ENMG abnormalities in a high percentage of patients who had treatment for CTS [24].

Scholten et al [26] carried out systematic review, for the Cochrane Database, to compare the efficacy of the various surgical techniques in relieving symptoms and promoting return to work or activities of daily living in patients with CTS. They found no strong evidence to support the need for replacement of the standard open carpal tunnel release by other existing alternative surgical procedures for the treatment of carpal tunnel syndrome. They found that none of the existing alternatives including endoscopic release offered significantly better relief from symptoms in the short- or long-term.

Neurolysis

In the past many surgeons used to do internal neurolysis as an adjunctive
procedure in operative treatment of carpal tunnel syndrome. It is now, however, no longer recommended, since several clinical studies have now failed to demonstrate any benefit from neurolysis [27,28].

Release of Guyon’s canal

Patients with carpal tunnel symptoms sometimes have paresthesias in the little finger. Some surgeons used to recommend simultaneous release of Guyon’s canal. This, however, is no longer recommended because there is evidence now which shows that the dimensions of Guyon’s canal enlarges with carpal tunnel release [29].

References

1. Sternbach G. The carpal tunnel syndrome. J Emerg Med. 1999 May-Jun;17(3):519-23.
2. Mitchell R, Chesney A, Seal S, McKnight L, Thoma A. Anatomical variations of the carpal tunnel structures. Can J Plast Surg. 2009;17(1):e 3–7.
3. Michelsen H, Posner MA. Medical history of carpal tunnel syndrome. Hand Clin. 2002; 18(2):257–68.
4. Falkiner S, Myers S. When exactly can carpal tunnel syndrome be considered work-related? ANZ J Surg. 2002;72(3):204–9.
5. Lozano-Calderon S, Anthony S, Ring D. The quality and strength of evidence for etiology: example of carpal tunnel syndrome. J Hand Surg Am. 2008;33(4):525–38.
6. Chammas M, Boretto J, Burmann LM, Ramos RM, dos Santos Neto FC, Silva JB. Carpal tunnel syndrome – Part I (anatomy, physiology, etiology and diagnosis. ). Rev Bras Ortop. 2014; 49(5): 429–36.
7. Andersen JH, Fallentin N, Thomsen JF, Mikkelsen S. Risk factors for neck and upper extremity disorders among computers users and the effect of interventions: an overview of systematic reviews. PLoS ONE. 2011;6(5):e19691.
8. Mackinnon SE. Pathophysiology of nerve compression. Hand Clin. 2002; 18(2):231–41.
9. Szabo RM, Slater RR Jr, Farver TB, Stanton DB, Sharman WK. The value of diagnostic testing in carpal tunnel syndrome. J Hand Surg Am. 1999 Jul;24(4):704-14.
10. Durkan J. A new diagnostic test for carpal tunnel syndrome. J Bone Joint Surg Am. 1991;73:535-538.
11. Katz JN, Stirrat CR. A self-administered hand diagram for the diagnosis of carpal tunnel syndrome. J Hand Surg Am. 1990 Mar;15(2):360-3.
12. Kuschner SH, Ebramzadeh E, Johnson D, Brien WW, Sherman R. Tinel's sign and Phalen's test in carpal tunnel syndrome. Orthopedics. 1992 Nov;15(11):1297-302.
13. Wang L. Electrodiagnosis of Carpal Tunnel Syndrome. Phys Med Rehabil Clin N Am  2013;24: 67–77.
14. Jablecki CK, Andary MT, So YT, Wilkins DE, Williams FH. Literature review of the usefulness of nerve conduction studies and electromyography for the evaluation of patients with carpal tunnel syndrome. AAEM Quality Assurance Committee Muscle Nerve. 1993;16(12):1392–414.
15. Witt JC, Hentz JG, Stevens JC. Carpal tunnel syndrome with normal nerve conduction studies. Muscle Nerve. 2004;29(4):515–22.
16. Atroshi I, Gummesson C, Johnsson R, Ornstein E. Diagnostic properties of nerve conduction tests in population-based carpal tunnel syndrome. BMC Musculoskelet Disord. 2003;4:9.
17. Redmond MD, Rivner MH. False positive electrodiagnostic tests in carpal tunnel syndrome. Muscle Nerve. 1988;11(5):511–8.
18. Seror P. Sonography and electrodiagnosis in carpal tunnel syndrome diagnosis, an analysis of the literature. Eur J Radiol. 2008;67(1):146–52.
19. Graham B. The value added by electrodiagnostic testing in the diagnosis of carpal tunnel syndrome. J Bone Joint Surg Am. 2008; 90(12):2587–93.
20. Girlanda P, Venuto C, Mangiapane R, et al. Local steroid treatment in idiopathic carpal tunnel syndrome: short and long–term efficacy. J Neurol 1993;240:187–90.
21. Dammers JW, Vermeulen M. Injections with methylprednisolone proximal to the carpal tunnel: randomized double blind trial. BMJ 1999;319:884–6.
22. Marshall  SC, Tardif  G, Ashworth  NL. Local corticosteroid injection for carpal tunnel syndrome. Cochrane Database of Systematic Reviews 2007, Issue 2. Art. No.: CD001554. DOI: 10.1002/14651858.CD001554.pub2.
23. Bland JD. Carpal tunnel syndrome. BMJ. 2007;335 (7615): 343–346.  doi: 10.1136/bmj. 39282.623553.AD.
24. Louie D, Earp B, Blazar P. Long-term outcomes of carpal tunnel release: a critical review of the literature. Hand (New York, NY). 2012; 7(3):242-246. 
25. Pensy RA, Burke FD, Bradley MJ, Dubin NH, Wilgis EF. A 6-year outcome of patients who cancelled carpal tunnel surgery. J Hand Surg Eur Vol. 2011 Oct;36(8):642-7.
26. Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003905. 
27. Lowry WE Jr, Follender AB: Interfascicular neurolysis in the severe carpal tunnel syndrome: A prospective, randomized, double-blind, controlled study. Clin Orthop 1988;227:251-254.
28. Mackinnon SE, McCabe S, Murray JF, et al: Internal neurolysis fails to improve the results of primary carpal tunnel decompression. J Hand Surg [Am] 1991;16:211-218.
29. Richman JA, Gelberman RH, Rydevik BL, et al: Carpal tunnel syndrome: Morphologic changes after release of the transverse carpal ligament. J Hand Surg [Am] 1989;14: 852-857.

Impingement syndromes of the ankle

                 Impingement syndromes of the ankle

                                         DR KS DHILLON

Introduction

A painful mechanical limitation of ankle movements caused by an osseous or soft-tissue abnormality is known as ankle impingement. Patients often present with chronic ankle pain of varying etiology. Ankle impingement syndrome, though rare, is one of the cause of chronic ankle pain [1]. 
There is no official classification for ankle impingement syndromes. The syndromes are described, depending on their location, as anterior, anterolateral, anteromedial, posterior, posteromedial, hindfoot extra-articular, and syndesmotic impingements [2].

Anterior ankle impingement

Anterior ankle impingement is usually seen in athletes such as football and soccer players, ballet dancers, gymnasts, and runners who are involved in activities that require repetitive ankle dorsiflexion.

Osseous anterior bony impingement occurs from osteophyte impingement of the anterior rim of the tibia and the talar sulcus. Repetitive forces are believed to lead to impaction-related microtrauma of the anterior chondral margin of the tibiotalar joint which over time leads to osteophyte formation from attempted repair with fibrosis and fibrocartilage proliferation [3]. The contact between opposing bone or the entrapment of soft tissues between the bones may produce pain. These osteophytes are located inside the joint and away from the capsular attachment.

Others believe that repetitive traction injury to the anterior joint capsule due to hyper plantar flexion leads to the formation of these osteophytes [4,5].

Although the anterior tibiotalar osteophytes are often referred to as “kissing osteophytes”, they do not actually overlap and abut. CT scan studies show that talar spurs usually lie medial to the midline of the talar dome and tibial spurs are usually located lateral to the midline [6]. There is a trough in the articular talar dome which usually “accepts” the tibial osteophyte during ankle dorsiflexion. Some refer to it as a “tram-track lesion” [7], and others refer to it as a “divot sign” [8]. Other studies have shown a high rate of  talar cartilage lesions (80.7 %) which correspond to the distal tibial osteophytes and also the presences of multiple loose bodies in these patients [9].

There is a triangular soft tissue mass which is composed of adipose and synovial tissues in the joint space in front of the ankle joint. This soft tissue mass can be compressed when dorsiflexion of the ankle exceeds 15° [10].

The presence of anterior osteophytes may further limit the space available for this soft tissue mass and cause entrapment, leading to chronic inflammation and synovitis[2]. Some of the other causes of anterior ankle pain include post-traumatic fibrous bands [11], thickened anterior tibiofibular ligaments [12,13], and synovial plica [14]. Although various types of lesions have been described, their exact etiology is not well understood.

Asymptomatic anterior tibiotalar spurs on lateral view x rays of the ankle may be present in 45% to 59% of professional athletes[15].

The clinical symptoms of anterior ankle impingement include pain and a subjective feeling of blocking on dorsiflexion. On examination, the dorsiflexion movements are painful and limited and occasionally a soft tissue swelling may be palpable [16]. The symptoms are usually due to degeneration of the joint rather than the spurs.

Usually plain x rays of the ankle are sufficient to detect the spurs. MRI of the ankle may show synovitis, effusion and bone marrow edema. However MRI is usually not necessary for anterior ankle impingement.

The mainstay of treatment is conservative with NSAIDs and rehabilitative  physiotherapy(16-18), but in resistant cases surgery appears to show  long-term benefit (16). Usually arthroscopic debridement of the spurs and soft tissues with a washout is carried out [16]. The prognosis depends on the severity of the degeneration of the joint [16]. A hundred percent to 77% excellent function after surgery at 6.5 years has been reported [16]. The evidence however remains weak.

Anterolateral Impingement

The anterolateral recess of the ankle is formed by the tibia posteromedially and the fibula laterally. Anteriorly and laterally lies the tibiotalar joint capsule, the anterior tibiofibular, anterior talofibular and the calcaneofibular ligaments.

Supination injuries, recurrent lateral ligament sprains and chronic lateral ligament instability can predispose a patient to anterolateral soft tissue impingement of the ankle. Chronic inflammation and hypertrophic changes of the synovial tissue occurs between the talus and the tibia [19]. Thickened synovial and scar tissue get entrapped in the anterolateral gutter  leading to pain and swelling after activity as well as limitation of ankle dorsiflexion and supination [20,21].

Rarely hypertrophy of the inferior portion of the anterior tibiofibular ligament and occasionally osseous spurs can cause anterolateral impingement [22,23].

Symptoms of anterolateral impingement include focal anterolateral pain
which is aggravated by supination or pronation of the foot. Examination usually shows anterolateral tenderness, swelling, pain on single-leg squatting, and pain on ankle dorsiflexion and eversion [22,23].
X rays of the ankle are usually of not much value in the diagnosis of anterolateral impingement. The role of MRI in the diagnosis is also controversial. MR arthrography has been able to detect abnormalities such irregular or nodular contour of the anterolateral soft tissues which correlated with anterolateral scarring or synovitis in the anterolateral recess of the ankle. However such finding are also seen in asymptomatic individuals [24]. Chondral defects, spurs, and laxity or rupture of the anterior talofibular ligament may also be seen in patients with anterolateral impingement.

Rehabilitative physiotherapy and NSAIDs usually relieve symptoms in most patients. Those who do not respond to conservative treatment are often treated with arthroscopic debridement of the joint. The published reports on the outcome of arthroscopic surgery for treatment of anterolateral impingement are level 4 retrospective studies[25 ] or involve small numbers of cases [26,27].

Anteromedial Impingement

The exact cause of anteromedial impingement is not know but it is believed to be caused by inversion or eversion injury leading to tearing of the anteromedial capsule and the tibiotalar ligament. Repeated microtrauma leads to synovitis and capsular thickening. Bony injury and cartilage damage may lead to spur formation with synovial and capsular thickening [1].

The clinical features include chronic anteromedial pain which is aggravated by ankle dorsiflexion. Examination shows anteromedial tenderness and limitation of ankle dorsiflexion and foot inversion [28,29].

MR arthrographic would show focal capsular and synovial thickening in
tibiotalar joint anterior to the tibiotalar ligament [29]. Bone spurs with anteromedial synovitis may also be seen.

There are no studies which document the effectiveness of conservative treatment in the treatment of anteromedial impingement syndrome. Neither has the outcome of steroid injections been well studied. Some authors recommend surgery (arthroscopic debridement) as the first line of treatment. Level 4 evidence (case series) shows excellent functional outcomes at a minimum of 2 years follow up [30].

Posterior Impingement

Posterior impingement is also known as the os trigonum syndrome and posterior tibiotalar compression syndrome [31]. Posterior impingement results from compression of soft tissues between posterior process of the calcaneus and the posterior tibia on plantar flexion of the ankle. The posterior talus contributes significantly to posterior impingement due to the presences of os trigonum or Stieda’s process in some patients.

Besides bony structures at the back of the ankle there are several ligamentous structures at the back of the ankle which include, the posteroinferior talofibular ligament, the transverse tibiofibular ligament, the tibial slip or the posterior intermalleolar ligament, and the posterior talofibular ligament [32].
Patients with posterior impingement syndrome usually present with pain at the back of the ankle on activities which involve extreme plantar flexion such as soccer, football, ballet and running downhill [31].

An acute plantar hyperflexion injury and chronic repetitive microtrauma are believed to lead to posterior impingement syndrome. Hypertrophy of the posterior tissue with compression leads to chronic pain at the back of the ankle. There may be damage to regional ligaments and tendon. Flexor hallucis tenosynovitis is often present in many patients [33].

Presence of a Stieda's process or an os trigonum is not diagnostic of impingement because these bony abnormalities are also present in asymptomatic individuals. A MRI can be useful in detecting bone marrow oedema within the talus, calcaneus or an os trigonum. It will also show synovitis and thickening of the posterior ligaments [32].

The first line of treatment is conservative, as with other impingement syndromes, and surgery can be carried out if conservative treatment fails. Surgery consists of arthroscopic debridement.

Posteromedial impingement 

The posteromedial joint space is bound by the medial malleolus and posterior tibiotalar ligament (PTTL) anteriorly and talar dome and posterior process of the talus laterally. Posteriorly it is bound by the posteromedial joint capsule, neurovascular bundle and flexor hallucis longus tendon.
The precipitating injury usually is plantar flexion, inversion and internal rotation trauma which leads to PTTL damage and synovitis ensues affecting the tibialis posterior, flexor hallucis longus and/or the flexor digitorum longus tendons [34].

It is one of the least common ankle impingement syndromes. Patients usually present with pain over the posteromedial aspect of the ankle with movements of the ankle.

Plain radiographs are of not much value in diagnosis of posteromedial impingement. A MRI would show abnormal pathology in the PTTL consisting of thickening and loss of the normal fibrillar pattern. Fluid collection, synovitis and irregular soft tissue may be seen in the posteromedial recess [35].
Treatment is usually conservatively, but surgical treatment may be contemplated in patients not responding to conservative treatment.

Extra-articular lateral hindfoot impingement syndrome (ELHIS)

The extra-articular lateral hindfoot impingement syndrome is not caused by trauma but results from a pathological tibialis posterior tendon which produces a flatfoot and hindfoot valgus deformity [36]. Commonly  impingement is seen between the lateral talus and calcaneus (talocalcaneal impingement) and also between the calcaneus and fibula (subfibular impingement) [36].

 Accessory anterolateral talar facet is also known to cause ELHIS. The accessory anterolateral facet can cause pathological impingement of the neck of the calcaneus in patient with flatfoot/hindfoot valgus deformity [37].

Repeated talocalcaneal and fibulocalcaneal impingement will lead to arthrosis at the contact points. Patients usually present with pain in the region of the sinus tarsi. Conventional radiography is useful in the diagnosis. Oblique x rays and valgus stress views are useful. Coronal oblique CT scans will also show the site of impingement. An MRI is useful for evaluating the degree of tibialis posterior tendon pathology. The MRI will also show cystic changes and bone marrow oedema within the lateral talus in addition to soft-tissue thickening between the fibula and the calcaneus and also show fibula tip oedema [36].

Initially treatment includes physical therapy, a period of immobilization, orthotics, and non-steroidal anti-inflammatory medications. In the event of failure of conservative treatment surgical intervention with preservation of the subtalar joint is carried out. Resection of the accessory anterolateral talar facet is carried out with correction of the hindfoot deformity. In patients with advanced arthritis subtalar arthrodesis is carried out [37].

Conclusion

Ankle impingement syndromes are an uncommon cause of chronic ankle pain. There is no classification for ankle impingement syndromes but they are named according to the location of the impingement around the ankle both anterior and posterior to the ankle. There are soft tissue and bony abnormalities involved in the pathology of impingement syndromes.
Symptoms with anterior impingement occur with terminal dorsiflexion and with posterior impingement on hyper plantar flexion.
The mainstay of diagnosis is history and physical examination. Imaging helps to confirm the diagnosis in most cases. Initially treatment is conservative, failing which open or arthroscopic surgery is carried out for treatment of impingement syndromes.
Although most authors claim good to excellent outcomes with arthroscopic surgery, the level of evidence however is low (level 4). Currently there is a lack of good quality outcome studies (level 1) in the literature for the treatment of impingement syndromes of the ankle.

References

1.  Robinson P, White LM. Soft-Tissue and Osseous Impingement Syndromes of the Ankle: Role of Imaging in Diagnosis and Management. RadioGraphics 2002; 22:1457–1471.
2. Lavery KP, McHale KJ, Rossy WH, Theodore G. Ankle impingement. Journal of Orthopaedic Surgery and Research. 2016;11(1):97. doi:10.1186/s13018-016-0430-x.
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Radiofrequency denervation for chronic axial back pain.

Radiofrequency denervation for chronic axial back pain.

                                   DR KS Dhillon 

What is radiofrequency denervation?

Radiofrequency denervation, radiofrequency neurotomy, and radiofrequency ablation are often used interchangeably. They all refer to a procedure that destroys the functionality of the nerve using radiofrequency energy.

There are primarily two types of radiofrequency ablation used in the treatment of axial back pain:

• A medial branch neurotomy which is used for treatment of spinal facet joint pain. 
• A lateral branch neurotomy which is used to treat pain from  the sacroiliac joints.

The facet joint is innervated by the medial branch of the dorsal rami from 2 adjacent spinal segments. The nerve supply of the SI joint is a contentious issue. The information is sparse and variable. For radiofrequency ablation (RFA) of the SI joint, the medial branch of L4, dorsal rami of L5, and lateral branches S1 and S2, are targeted.

The procedure involves setting up of an IV line, sedation, skin preparation, local anesthetic injection, fluoroscopic guided insertion of radiofrequency needle to the required site and passage of a small current to confirm the targeted nerve, numbing of the target nerve with local anesthetic, passage of radiofrequency waves to heat the tip of the needle and creating a heat lesion to denervate the nerve.

Efficacy of radiofrequency denervation for facet joint pain

Radiofrequency facet joint denervation procedures for the treatment of chronic low back pain have been in common use for more than 3 decades.  The efficacy of the procedure, however, has never been conclusively established.

van Wijk et al [1], in 2005, published the outcome of a multicenter, randomized, double-blind, sham treatment controlled trial to determine the efficacy of radiofrequency facet joint denervation. They had a total of 81 patients who were randomized to undergo radiofrequency facet joint denervation or sham treatment. A twice weekly recording of VAS, physical activity and analgesic intake determined the primary outcome. The secondary outcome measure included the global perceived effect (complete relief, >50% relief, no effect, pain increase), and the SF-36 Quality of Life Questionnaire.They carried out the first evaluation 3 months after treatment. There were no dropouts in the first evaluation. They found that the combined outcome measure showed no differences between radio- frequency facet joint denervation and the sham group.The VAS improved in both groups. Only the global perceived effect improved after radiofrequency facet joint denervation. They concluded that only in selected patients, radiofrequency facet joint denervation appears to be more effective than sham treatment but overall there is no benefits from radiofrequency denervation in treatment of chronic low back pain.

Gofeld et al [2] did a prospective clinical audit for quality in 209 patients with chronic back pain who were treated with radiofrequency denervation of the lumbar zygapophysial joints. The patients were screened and those with multiple unrelated painful sites, significant psychopathology and those with unrealistic goals were not included in the study. One hundred and seventy four patients (83%) completed the study. The patients were asked to complete a questionnaire at 6 weeks, 6 months and at 12, and 24 months following the procedure. They were asked to estimate the total perceived pain reduction on a scale of 0% to 100%. Improvement of pain more than 80% was graded as excellent and between 80% to 50% was graded as good. Pain improvement less than  50% and pain relief lasting less than 6 months were considered as treatment failure.

In 55 (31.6%) patients, the treatment was a failure. One hundred and nineteen (68.4%) patients had good to excellent pain relief at 6 months follow up. Of the 119 patients, 81 (96.4%) reported pain relief for 6–12 months, 36 (42.8%) for 12–24 months, and 2 (2.4%) for more than 24 months. The median pain relief among all eligible 174 patient was 9 month.

All the 119 patients with a positive response were able to increase their physical activities, and 99 (83.2%) of these also decreased their consumption of analgesics (not stopped use of analgesics) and in 20 other patients with a positive response the use of analgesics remained unchanged.
These figures do, however, raises doubts about the efficacy of the procedure which can be associated with complication, because the procedure did not eliminate the use of analgesics and only 2.4% of patients had relief after 24 months.

Lakemeier et al [3] carried out a randomized, controlled, double-blind trial, to compare intraarticular lumbar facet joint steroid injections and lumbar facet joint radiofrequency denervation in the treatment of low back pain. The Roland-Morris Questionnaire was the primary endpoint and the secondary endpoints were the visual analog scale and the Oswestry Disability Index. The outcome assessments were performed at baseline and at 6 months. The study involved fifty-six patients where 24 of 29 patients in the steroid injection group and 26 of 27 patients in the denervation group completed the 6-month follow-up. There was pain relief and functional improvement in both groups and there were no significant differences between the 2 groups for both the primary endpoint and secondary endpoints.

This study, if valid, would encourage the use of intraarticular lumbar facet joint steroid injections rather than joint radiofrequency denervation for treatment of lumbar facet pain, and in doing so, resources can be saved.

Maas et al [4] did Cochrane Database Systematic Review in 2015 to assess the effectiveness of RF denervation procedures for the treatment of patients with chronic low back pain.The authors found that there is no high-quality evidence which suggests that RF denervation provides pain relief for patients with chronic low back pain. They also found no convincing evidence to show that such treatment improves function. They concluded that the current evidence for RF denervation for chronic low back pain is very low to moderate in quality and high-quality evidence does not exist.

Juch et al [5] conducted three pragmatic multicenter, non blinded randomized clinical trials to assess the effectiveness of radiofrequency denervation in patients with chronic low back pain originating from the facet joints, sacroiliac (SI) joints and or the disc. They found that radiofrequency denervation combined with a standardized exercise program resulted in either no improvement or no clinically important improvement in chronic low back pain compared with a standardized exercise program alone. They concluded that their findings do not support the use of radiofrequency denervation to treat chronic low back pain from the facet and SI joints and the disc.

Lee et al [6] in 2017 carried out a meta-analysis of 7 RCT for a total of 454 patients with low back pain due to facet joint disease of the lumbar spine. Comparison was made between patients who had radiofrequency denervation and those who had control/sham treatments. The follow up was upto 1 year. Two hundred and thirty one patients had radiofrequency ablation and 223 patients had control treatments such as sham or epidural block procedures. At 1 year follow up, there was a greater improvement in the radiofrequency denervation group and the mean difference for VAS scores between the two groups was 3.55.The authors concluded that radiofrequency denervation produced significant reduction in low back pain originating from the facet joints compared with sham procedures or epidural nerve blocks.

The systematic reviews (SRs) indicate that there is conflicting evidence regarding the benefits of radiofrequency denervation for facet joint pain, which makes it difficult to recommend it for treatment of chronic low back pain. Most of the studies included in the  SRs were usually small with a mix of randomized and non-randomized studies. The studies did not document well the adverse events and complications related to the radiofrequency denervation procedure. The primary studies had small population size and were of short duration which makes it difficult to determine the long term benefits associated with the procedure.

Since there is no long term outcome data available to determine the benefits of the procedure, the literature does not support the use of the procedure to treat chronic low back pain.

References

1. van Wijk RM, Geurts JW, Wynne HJ, Hammink E, Buskens E, Lousberg R, Knape JT, Groen GJ. Radiofrequency denervation of lumbar facet joints in the treatment of chronic low back pain: a randomized, double-blind, sham lesion-controlled trial. Clin J Pain. 2005 Jul-Aug;21(4):335-44.
2. Gofeld M, Jitendra J, Faclier G. Radiofrequency denervation of the lumbar zygapophysial joints: 10-year prospective clinical audit. Pain Physician. 2007 Mar;10(2):291-300.
3. Lakemeier S, Lind M, Schultz W, Fuchs-Winkelmann S, Timmesfeld N, Foelsch C, Peterlein CD. A comparison of intraarticular lumbar facet joint steroid injections and lumbar facet joint radiofrequency denervation in the treatment of low back pain: a randomized, controlled, double-blind trial. Anesth Analg. 2013 Jul;117(1):228-35.
4. Maas ET, Ostelo RW, Niemisto L, Jousimaa J, Hurri H, Malmivaara A, van Tulder MW. Radiofrequency denervation for chronic low back pain. Cochrane Database Syst Rev. 2015 Oct 23;(10):CD008572.
5. Juch JNS, Maas ET, Ostelo RWJG, Groeneweg JG, Kallewaard JW, Koes BW, Verhagen AP, van Dongen JM, Huygen FJPM, van Tulder MW. Effect of Radiofrequency Denervation on Pain Intensity Among Patients With Chronic Low Back Pain: The Mint Randomized Clinical Trials. JAMA. 2017 Jul 4;318(1):68-81.
6. Lee CH, Chung CK, Kim CH. The efficacy of conventional radiofrequency denervation in patients with chronic low back pain originating from the facet joints: a meta-analysis of randomized controlled trials. Spine J. 2017 Nov;17(11):1770-1780.