Epidemiology

• One of the most common and frequently diagnosed entrapment neuropathies
  
  
  
  • Accounts for up to 90% of entrapment neuropathies
    
  • Prevalence in the US population up to 5% of the general population
    
    
    
    • Estimated lifetime risk of 10%
      
    • Females affected more frequently than men
      
    • Peak age range 40–60 years
    
    
  • Risk factors include prolonged wrist flexion or extension, repeated use of flexor muscles, and exposure to vibration
    
    
    
    • Systemic medical conditions i.e. diabetes, hypothyroidism, obesity, pregnancy, vitamin toxicity or deficiency can predispose
      
    • Many cases remain idiopathic

Pathology

• Median nerve entrapment is caused by chronic pressure at the level of the carpal tunnel
  
• Compression of the median nerve is secondary to surrounding structures: carpal bones, flexor tendons, and the fibrous transverse carpal ligament leading to median nerve dysfunction
  
  
  
  • Carpal tunnel anatomy (Figure 1.1)
    
    
    
    • Superiorly: transverse carpal ligament
      
    • Posteriorly: carpal bones
      
    • Nine flexor tendons: (four) flexor digitorum profundus, (four) flexor digitorum superficialis, flexor pollicis
      
    • Median nerve
  
  
• Repetitive compressive injury to the median nerve leads to demyelination
  
  
  
  • Blood flow may also be interrupted, altering the blood–nerve barrier

Clinical Presentation

• Symptoms may include tingling and numbness, in the distribution of the median nerve (first three fingers and radial aspect of the fourth finger); pain involving the entire hand, decreased grip strength, and reduced dexterity
  
  
  
  • Symptoms occasionally worse at night (awakenings with paresthetica nocturna: sensation of tingling, burning or numb hand possibly secondary to flexion of wrist at night)
  
  
• Patients with carpal tunnel syndrome (CTS) occasionally report subjective swelling of the hands and/or wrists
  
• Atrophy of the thenar eminence occurs in later stages (this finding is associated with poor response to surgical decompression)

Diagnosis

• Combination of the clinical history, examination, provocative tests, electrodiagnostic studies
  
  
  
  • Phalen’s test is positive when flexion at the wrist for 60 seconds causes pain and/or paresthesias in median nerve distribution
    
    
    
    • Sensitivity ranges from 67–83%
      
    • Specificity ranges from 40–98%
    
    
  • Tinel’s test is positive when tapping over the volar surface of the wrist (course of median nerve) causes pain and/or paresthesias in the distribution of the median nerve
    
    
    
    • Sensitivity ranges from 48–73%
      
    • Specificity reported as high as 100%
    
    
  • Electrodiagnostic studies lack standardized diagnostic criteria currently, making them inadequate as a universally recognized gold standard
    
    
    
    • Nerve conduction studies provide objective information regarding the median nerve across the carpal tunnel
      
      
      
      • Findings include prolonged motor and sensory latencies of median nerve
        
      • Reduction in median nerve compound motor or sensory action potential amplitude
        
      • Reductions in sensory and motor conduction velocities
        
      • Rules out other polyneuropathies included in the differential diagnosis
    
    
  • Ultrasonography may reveal flattening of the median nerve within the tunnel and bowing of the flexor retinaculum
    
    
    
    • Cross-sectional area of the median nerve is the most predictive of CTS; it has also been used in the classification of the severity of CTS
    
    
  • Magnetic resonance imaging assists in the determination of the severity of nerve compression; it is also helpful in observing anatomical structures that may be contributing to symptoms, i.e. ganglion cysts, bony deformities
    
    
    
    • Swelling of the median nerve and increased signal intensity on T2- weighted images assist in diagnosing CTS

Treatment

• Mild to moderate symptoms
  
  
  
  • Oral anti-inflammatories
    
  • Oral corticosteroids may be effective in reducing edema and tenosynovitis associated with CTS
    
  • Carpal bone mobilization and hand splints are often first-line treatment options
    
  • Corticosteroid injection along the proximal wrist crease just ulnar to the palmaris longus tendon provides clinical improvement, however benefit beyond 1 month was not shown in a systematic review
    
  • Ultrasound therapy
  
  
• Moderate to severe symptoms
  
  
  
  • Acupuncture therapy has been reported to improve median nerve function
    
  • Carpal tunnel release (CTR)
    
    
    
    • Surgical procedure to increase space in the carpal tunnel and reduce pressure on the median nerve, via division of the transverse carpal ligament
      
    • Good to excellent long-term outcomes following CTR in up to 90% of reported cases
      
    • Surgical treatment has been reported to demonstrate better long-term response when compared to splinting

Differential Diagnosis

• Cervical radiculopathy
  
• Proximal median neuropathy
  
• Thoracic outlet syndrome
  
• Central nervous system (CNS) disorders

Epidemiology

• Most common arthritis
  
• A leading cause of chronic pain and disability in older adults

Commonly Involved Joints

• Hand – most commonly involved in OA – distal interphalangeals (DIPs), proximal interphalangeals (PIPs), first carpometacarpal (CMC)
  
• Feet – first metatarsophalangeal (MTP), subtalar joint
  
• Knee
  
• Hip
  
• Spine
  
• Rarely affects elbow, wrist, ankle – look for history of trauma, congenital abnormality, systemic or crystalline disease

Definition

• OA can be defined pathologically, radiographically, or clinically
  
• Radiographic OA has long been considered the reference standard for epidemiology
  
  
  
  • Not all subjects with radiographic OA are symptomatic and not all with symptoms have radiographic OA

Risk Factors

• Age – the strongest risk factor, most commonly age >40 years
  
• Females
  
• Obesity – the strongest modifiable risk factor
  
• Previous injury
  
• Family history (genetic predisposition)
  
• Joint malalignment (mechanical factors)

Pathogenesis

• Caused by an interplay of multiple factors – joint integrity, genetics, local inflammation, mechanical forces, cellular and biochemical processes
  
• Abnormal remodeling of joint tissues is driven by a host of inflammatory mediators within the joint
  
• OA pathogenesis is now thought of as an active response to injury rather than a degenerative process
  
  
  
  • Degradation of matrix and articular cartilage
    
    
    
    • Chondrocytes become “activated” and increase production of matrix proteins and matrix-degrading enzymes during inadequate repair response
      
      
      
      • Aggrecanases, collagenases, serine and cysteine proteinases, matrix metalloproteinase (MMP)-3, MMP-13, ADAMTS-5 are all reported to play a role
    
    
  • Thickening of the subchondral bone
    
    
    
    • Bone remodeling may be initiated at sites of local bone damage resulting from excessive repetitive loading
    
    
  • Formation of osteophytes
    
    
    
    • At joint margins and entheseal sites – new bone is added by endochondral ossification, leading to osteophyte formation
    
    
  • Variable degrees of inflammation of the synovium
    
    
    
    • Synovial infiltrates have been identified in many OA patients, though lower in grade than in rheumatoid arthritis (RA)
      
    • Prevalence of synovitis increases with advancing age
      
    • Interleukin (IL)-1 beta and tumor necrosis factor (TNF) alpha suppress matrix synthesis and promote cartilage catabolism, IL-17 induces chemokine production by synovial fibroblasts and chondrocytes
    
    
  • Degeneration of ligaments, menisci in the knee, and hypertrophy of the joint capsule, as any meniscal or ligamentous injury predisposes to the development of OA

Symptoms

• Hand
  
  
  
  • Pain on usage
    
  • Mild morning or inactivity stiffness, usually lasting <30 minutes
    
  • Characteristic sites – DIPs, PIPs, base of the thumb
  
  
• Knee and hip
  
  
  
  • Usage-related pain
    
  • Often worse toward the end of the day
    
  • Pain relieved, usually incompletely, with rest
    
  • Mild morning or inactivity stiffness (gelling)
    
  • Advanced OA – may have rest or night pain
    
  • OA symptoms are often episodic or variable in severity and slow to change

Physical Examination

• Hand
  
  
  
  • Heberden’s (DIPs) and Bouchard’s (PIPs) nodes
    
  • Squared appearance to the first CMC is classic
  
  
• Feet
  
  
  
  • First MTP involvement may result in hallux valgus or hallux rigidus
  
  
• Knees
  
  
  
  • Tenderness to palpation of joint
    
  • Crepitus
    
  • Joint effusion
    
    
    
    • Synovial fluid in OA typically exhibits
      
      
      
      • Normal viscosity
        
      • Mild pleocytosis (WBC <2000/mm³)
    
    
  • Osteophytes – may have palpable bony enlargements at periphery of joint
    
  • Restricted movement and range of motion
  
  
• Hip
  
  
  
  • Hip pain worsened with internal or external rotation
    
  • Anterior and inguinal pain generally indicative of true hip joint involvement
    
  • Check both hips, as ∼20% have bilateral OA
    
  • Full exam should also include evaluation for referred pain sources
    
    
    
    • Trochanteric bursitis
      
    • Lumbosacral spine
      
    • Knee pathology

Osteoarthritis Treatment