Evaluation and treatment of the cervical spine

Copyright 1998-2015 The Manual Therapy Institute PLLC

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Copyright 1998-2015 The Manual Therapy Institute PLLC


The cervical vertebrae are the smallest of the moveable vertebrae. The 1st, 2nd and 7th have special features and will be considered separately.

The typical cervical vertebra runs from C3 to C6. It has a small but relatively broad body. The body’s anterior surface is convex transversely. The cranial surface of the body is concave transversely, convex A-P, with marked bilateral lips. The inferior surface is convex transversely and concave A-P.
Uncinate processes grow upwards from the upper aspects of the lateral parts of each vertebra (C3 to T1). Between its tip and the lower lateral surface of the vertebral body above they form the uncovertebral joints. The uncovertebral joints are present from C2-3-C7-T1. The most prominent uncinate process is found at C2-3. They start to develop at 6-9 years and are fully developed at 18 years. The medial border is formed by the disc, the lateral border by ligaments. The joint surfaces are covered with hyaline cartilage. The uncovertebral joints enhance the stability of the cervical spine. They act as a “rail” to guide flexion and extension. It limits sidebending. They are frequently affected by spondylotic changes.
The vertebral foramen is large and roughly triangular. The laminae are long and narrow.

The spinous processes are short and bifid, with the terminal tubercles often unequal in size. The transverse processes face lateral, anterior and inferior. They have a gutter on top, through which the nerve root runs. Each cervical vertebra has a transverse foramen through which the vertebral artery runs.

The superior and inferior articular processes form (when articulated), the articular pillar. The superior articular facet faces posterior and cranial, the inferior articular facet faces anterior and caudal.

The atlas

It is unique in that it lacks a body. It is a bony ring, made up of 2 lateral masses connected by a short anterior and a longer posterior arch. The anterior arch is slightly convex. The anterior tubercle serves as an attachment for the ALL. On the posterior side of the anterior arch is a small facet where the dens articulates with C1. The posterior tubercle is a rudimentary spinous process functioning as an attachment for the ligamentum nuchae. The transverse processes are very long, up to 90 mm. in males. The superior articular facets are concave and face in a medial, cranial direction. The inferior articular facets are convex and face medial and caudal.


C2 is a transitional vertebra. The dens projects vertically. It functions as an axis for C1-2 rotation. The transverse processes are small and blunt at their tips with single tubercles. The spinous processes are still bifid. The superior articular facets are concave in their bony configuration, but covered with cartilage, they are convex. The inferior articular facets are like in the mid cervical spine, facing anterior and caudal.


C7 is a transitional vertebra as well, connecting the mobile cervical spine with the much more stable thoracic spine. It has a long spinous processes (although T1 is usually just as prominent), with a single tubercle at its end.


The cervical disc should not be regarded as a smaller version of the lumbar disc. It has less soft nuclear material, and the nucleus only really exists in childhood and young adulthood. By 40 years of age, there is no gelatinous nucleus anymore; rather the central region of the disc is composed of fibrocartilage. Therefore, nuclear prolapse is less likely, except in severe traumatic incidents. The annulus fibrosis is not a ring-like structure of lamellae. Rather, it is a discontinuous structure, which is made up of 2 distinct portions. The anterior annulus is crescent shaped and runs between the uncinate processes. It is well developed and thick at the midline, tapering as it approaches the anterior margin of the uncinate processes. The posterior annulus is a small structure represented by a few vertically oriented fibers located close to the median plane at the posterior aspect of the disc. It is thin, not more than 1 mm in depth. The posterolateral aspect of the disc therefore lacks the support of the annulus fibrosis.

Horizontal fissures or clefts begin developing between 9-14 years of age, until they completely transect the posterior two-thirds of the disc. This is considered to be normal anatomy of a cervical disc, which together with the absence of a substantial posterior annulus, facilitate axial rotation. The cervical disc bears less weight then the lumbar disc. As a degenerative phenomenon, lumbar discs usually herniate posterolateral. For the fissured cervical annulus it’s more common to show a generalized bar-like, posterior bulge.

Vertebral artery

The vertebral artery arises from the first part of the subclavian artery and passes upward on the longus colli to enter the foramen transversarium of C6. Occasionally it may enter the bone at the 5th, 4th or 7th cervical transverse foramen. It then ascends from C6 to C1. After emerging through the transverse foramen of C1, it winds around the articular pillar and together with the 1st cervical nerve and veins pierces the posterior atlanto-occipital membrane to enter the cranium through the foramen magnum. On the anterior side of the brainstem it joins its fellow to form the basilar artery. The vertebral arteries contribute about 11 percent of the total cerebral blood flow, the remaining 89 percent being supplied by the carotid system.
Ligaments cervical spine

Atlanto occipital joint ligaments
Joint capsule

Thin and loose. Surrounds the condyles of the occipital bones, connects them with the articular processes of the atlas.

Anterior atlanto occipital membrane

Connects the anterior part of the foramen magnum to the anterior arch of C1. It is thought to be a continuation of the ALL. May provide some A-P stability when both anterior and posterior A-O membranes are intact.

Posterior atlanto occipital membrane

Connects the posterior ring of C1 to the occiput at the foramen magnum. Broad and thin.

The anterior and posterior membranes prevent anterior and vertical displacement of C1 and C2.
Ligaments connecting C2 with occiput
Tectorial membrane

Continuation of PLL. Runs from the body of C2 up over the posterior portion of the dens and then makes a 45-degree angle in the anterior direction as it attaches to the anterior edge of the foramen magnum. It limits flexion, extension and vertical translation. Unable to prevent any anterior dislocation.

Alar ligament

A pair of ligaments attached to the dorsolateral surfaces of the tip of the dens. Each runs obliquely to the medial surfaces of the occipital condyles. They primarily limit rotation. The left one limits rotation of C1 and the head to the right, and vice versa.

Apical ligament

Connects the apex of the dens to the anterior edge of the foramen magnum. It is a fairly strong structure of elastic consistency. It contributes little to upper cervical spine stability.

Ligaments of the atlanto axial joint
Anterior atlanto axial membrane

Connects C1 to C2 anteriorly. Strengthened at mid line by a rounded cord

Posterior atlanto axial ligament

Broad thin membrane. Attaches to the posterior ring of the atlas and the axis. The posterior A- O and A-A membrane are anatomically analogous to the yellow ligament. However they are considerably different in physical properties. The yellow ligament is first present between C2-3. If present higher up, the highly elastic but still rather stiff yellow ligament would never allow the considerable amount of rotation currently present in the upper cervical spine (80 degrees). So stability is sacrificed for ROM.

Cruciate ligament

The major portion of this ligament is the transverse ligament, which is the most important ligament in the upper cervical spine. There is an ascending and a descending part, which are triangular shaped. The ascending portion attaches to the anterior edge of the foramen magnum, the descending part attaches to the body of C2. They are 3-4 mm thick. The ascending and descending part have little importance in controlling physiological motion, but they do check inferior/superior displacement of the transverse ligament.

Transverse ligament

Most important ligament in upper cervical spine, it is the number one stabilizer. It’s 7-8 mm thick. It attaches on the medial surface of the lateral mass of the atlas. It keeps the dens in contact with the anterior arch of C1. Anterior dislocation of C1 on C2 can only occur with insufficiency of the transverse ligament.

Remaining cervical spine ligaments
Nuchal ligament

Distinct band that runs from the posterior border of the occiput to the SP of C7. Anteriorly it attaches to the SP’s of the cervical vertebrae and the interspinous ligaments. Its precise role has not been identified yet. It may play an important role in the clinical biomechanics of the neck. One hypothesis is that it plays a major proprioceptive role in the functioning of the erector spinae muscles. Another hypothesis is that it provides A-P stability at C1-4 due to specific fiber attachment.

Anterior longitudinal ligament

Continuation of the ligament that runs the entire length of the spine. Well developed in the thoracic and lumbar regions. Described as a thin, translucent structure in the cervical spine. Little is known about the mechanical properties of this structure in this region of the spine.

Anatomic considerations regarding upper cervical spine stability
The O - A joint is relatively unstable. The anatomical structures providing stability are the cup shaped joints and the capsules, along with the A-O membranes. The role of the ligamentum nuchae as a stabilizer is controversial. Additional stability is gained from the tectorial membrane, the alar and apical ligaments. Dislocations of this joint are usually fatal.

At C1 - 2 the facet joints are bi convex and are held together by a loose capsule designed to permit a large range of motion. Consequently, joint congruency and the joint capsules contribute little to the stability of the joint. The mechanical stability is provided through the dens and the ring formed by the anatomic structures surrounding it. These consist of the bony portion of the dens anteriorly and laterally and the transverse ligament posteriorly. All the other anatomic structures play a secondary role in the stability of this joint. The strong yellow ligament is not present between C1-2. Instead there is the weaker atlanto axial membrane.

External occipital protuberance

Bony prominence at the middle of the occiput. Easily palpable and its size varies greatly. From here the lateral bony ridge of the occiput (linea nuchae) can be felt.

Mastoid processes

Lies beind the ear at each side of the occiput. Insertion of the SCM.

C1 transverse process

Can be palpated 1cm distal and slightly anterior to the mastoid process.

Styloid processes

Palpable right below the earlobe, between the mastoid process and the angle of the mandible. Normally very tender on palpation, so be gentle.

Transverse processes

Palpable in the lateral neck region. Located more anterior than what you would expect. Place your palpating fingers in the lateral neck region, just in front of the trapezius, and exert pressure in a medial direction.

Spinous processes C 2 - C 7

C1 does not have a spinous process. The first SP is C2. The C3-5 SP’s are difficult to palpate. C6-7 are easy to palpate. The latter two can be identified during neck extension: the SP of C6 “disappears”. It is often said that C7 has the most prominent SP, but often T1 can be more prominent. So don’t use the “most prominent SP” argument as the only reference point in identifying C7 SP.

Articular pillar

Start by palpating the SP of C2. Move one fingerswidth laterally. Gently palpate in a cranial/caudal direction, and you should feel “peaks and valleys”. The peaks are the facet joints.

Longus colli

Attaches to the anterior surface of the vertebrae from C 1 - T 3. Three - layered muscle. In the upper cervical area, start your palpation on the medial side of the SCM, in the mid/lower cervical are, start lateral from the SCM and deflect the muscle as you move medially. Be gentle when palpating the longus colli. Make sure not to compress the carotid artery when palpating. You need to palpate the muscle more medially than what you would expect at first.

Scalenus musculature

Palpable in the lateral cervical area between the upper trapezius and the SCM

First rib


  • Winkel, D. Diagnosis and Treatment of the Spine. Aspen Publishers, Gaithersburg MD 1996

Biomechanics and arthrokinematics

Approximate ROM for the Cervical Spine
Data are compiled from multiple sources. Because of the large range and variability in the data presented in the literature, the actual values listed in this table are more useful for appreciating the relative kinematics among joints, and less as a strict objective guide for evaluating movement in patients.


Flexion and Extension




Flexion 5

Extension 10

Minimal, conjunct



Flexion 5

Extension 10




Flexion 35-40

Extension 55-60



Total C- Spine

Flexion 45-50

Extension 75-80



The upper cervical joints allow the head to move on the neck. The mid cervical joints position the head in space.

Sidebending and rotation are coupled opposite in C 0 - C 1. In the mid cervical spine they are coupled to the same side.
C0 - C1

The articular surfaces of the occipital condyles are bi-convex. The superior articular surfaces of C 1 are bi - concave and face superior and medial. The long axes of the superior facets of the atlas converge anteriorly.

The joint has 2 degrees of freedom: flexion/extension in the sagittal plane and sidebending in the frontal plane. Rotation is conjunct to the opposite side of sidebending.
During flexion, both convex occipital condyles glide in the opposite direction of the movement of the occiput (posterior).
During extension, both occipital condyles glide in the opposite direction of the movement of the occiput (anterior).
During right side bending, the right C 0 moves in medial / inferior / anterior direction. The left C 0 moves in lateral / posterior / superior direction. This creates a conjunct left rotation at this level as well.
MIA has nice LPS “

C 1 - 2

The inferior articular facets of C 1 are convex, as are the superior articular facets of C 2. Due to this shape, no side bending is possible. Rotation is the main movement, while flexion / extension is fairly minor. The axis of movement during rotation of C 0 - 2 is through the dens.
A synovial joint is present between the posterior surface of the anterior arch at atlas and the anterior surface of the dens. There is also an articulation between the posterior surface of the dens and the anterior surface of the transverse ligament.
On right rotation, the right facet of C1 glides in posterior direction. The left facet glides in anterior direction. On left rotation, the opposite occurs.

During flexion, both facet surfaces of C1 roll anterior and glide posterior. The anterior arch of C1 glides in a caudal direction on the anterior surface of the dens. During extension, the opposite occurs.

C 2 - 3

C 2 is a transitional vertebra. The superior articular joint surfaces are part of the upper cervical spine, whereas the lower articular surfaces are of the mid - cervical variety.

C 2 - C 7

The articular surfaces of the superior articular facet are slightly convex and face cranial and posterior. The articular surfaces of the inferior articular facet are slightly concave and face caudal and anterior. The facet orientation in the mid cervical spine is approximately 45 degrees to the horizontal.
Flexion: the facets move up and forward

Extension: the facets move down and back

Sidebending: during right sidebending, the right facet moves down and back, the left facet up and forward.

Rotation: during right rotation, the right facet moves down and back, the left up and forward.
Differential Diagnosis

Taking patients on referral even if they have been X rayed is no guarantee that there is not a fracture present. The problem is of course compounded in a direct access environment. Apart from direct trauma, there is the possibility of stress- and pathological fractures. The clinical recognition of a fracture can be very difficult and great care must be taken with patients with complaints of deep sharp pain. Among some of the clinical indicators of a fracture are the following:

  • Trauma

  • Immediate posttraumatic onset of severe pain

  • Cracking noise at time of injury

  • Posttraumatic hemarthrosis

  • Crepitus

  • Strong multidirectional spasm

  • Severe pain on compression

  • Bone tenderness

  • Pain on vibration

  • Painful weakness on isometric testing

  • Severe bruising

  • Loss of normal contour

Is there an evidence based way to determine if a patient needs a radiograph? The Canadian cervical spine CPR (JAMA 2001) helps to determine if the patient actually needs radiography.

1. Does the patient display any high risk factors that mandate radiography?

  • Patient age>65

  • Dangerous injury mechanisms: fall from > 1 meter or 5 stairs; axial load to the head; MVA >100km/hr; bike collision.

  • Paresthesiae in the extremities

2. If that is the case, radiographs are warranted. If this is not present, proceed to ROM testing. Keep in mind the following low risk factors:

  • Simple rear end MVA

  • Delayed onset of neck pain

  • Absence of midline C spine tenderness

  • Patient is ambulatory

  • Patient is able to sit in the waiting room

If that is not the case, radiographs are warranted. If this is the case though, proceed to seated ROM testing.

3. Is the patient able to actively rotate the head 45 degrees to the left and to the right? If that is not the case, radiographs are warranted.

Cervical Spinal Stenosis

Prevalence of neck pain increases in a linear fashion from age 20-60

Spondylosis, DJD is seen in 10% of 25 yrs old, and 95% of 65 yrs old

Spinal stenosis is a narrowing of the spinal canal, either central or lateral. It is associated with spondylosis. It is the most common cause of spinal cord disorders in patients >55 yrs

There are three forms of cervical spinal stenosis:

  • Degenerative: osteophyte formation, degenerative disc, hypertrophy of the ligamentum flavum

  • Congenital: present due to spinal development

  • Traumatic: single incident

Spinal canal mechanics

  • In flexion the spinal canal widens by 31%

  • In extension the spinal canal diameter decreases and narrows by 20%. The cord and roots can become pinched between disc anteriorly, and by buckling ligamentum flavum and facet osteophytes posteriorly

  • In rotation there is ipsilateral neuroforaminal narrowing, and contralateral neuroforaminal widening


  • Chronic and slowly progressing

  • May have focal radicular type symptoms

  • May present with spondylotic myelopathy

Treatment options for spinal stenosis

  • Pharmacology

  • Surgery

  • Conservative


NSAIDs, help reduce inflammation and are more effective than placebo in back pain. Opioids should be used for patients with moderate to severe persistent pain. Neuropatic pain may be opioid resistant. Muscle relaxers are shown to reduce pain and improve function spinal pain patients. Epidural steroid injections provide up to 6 months of pain reduction.


  • Anterior approaches report a success rate as high as 67%, 55% long term. Increased stability is noted.

  • Posterior approaches report significant immediate neurologic improvement in up to 97%, 60% long teerm success. Long term adjacent segment deterioration is noted in 40%. There is decreased success with advanced cases.

  • Factors negatively impacting surgical improvement: age>50, duration of symptoms> 1 year, involvement of multiple levels, smoking


  • Cervical collars: no available long term evidence, some short term improvement

  • Acupuncture: lack of evidence, may provide short term pain relief

  • Physical therapy: limited quality evidence. Treat the effects of immobilization and movement restriction. Functional improvement with neuromuscular control exercises. Improved outcome measures have been reported in a case series with treatment consisting of ICT and thoracic manipulation. Traction was performed for 15-20 min at 16-24# in 24 degrees of cervical flexion. Treat the impairments within the limits of symptom exacerbation. Based on the fact that flexion increases the diameter of the spinal canal and widens it by 31%, it stands to reason to emphasize a flexion biased protocol.

Conservative treatment vs surgery

  • 1 and 10 year follow up: no significant difference

  • Recommended 3 months trial of non-operative treatment

  • Surgery recommended for moderate to severe cases with progression of neurologic symptoms

Cervical myelopathy

Cervical myelopathy is spinal cord compression in the spinal canal caused by osteophytes or disc degeneration.

  • Sensory disturbance of the hands

  • Muscle wasting of hand intrinsic muscles

  • Unsteady gait

  • Positive Hoffman’s and/or Babinski

  • Hyperreflexia

  • Bowel and bladder disturbances

  • Bilateral or quadrilateral limb paresthesiae and/or weakness

Cervical myelopathy is classified on the basis of gait dysfunction. Patients with a grade 1 CCM have upper motor neuron signs with a normal gait. Grade 1 is considered mild CCM. Grade 2-5 are characterized by worsening gait disturbances and are considered to be moderate to severe CCM. Moderate to severe CCM has a poor prognosis and is generally treated surgically. Conservative management has been recommended for patients with mild CCM.

Cook et al identified a cluster of findings useful in identifying patients with this complex diagnosis in similar patient populations. This study found clustered combinations of clinical findings that could rule in and rule out CSM

  1. Gait deviations

  2. Positive Hoffman’s

  3. Inverted supinator sign

  4. Positive Babinski

  5. Age >45 years

When 3/5 positve, CSM could be ruled in (+LR 30.9). When 1/5 positive, CSM could be ruled out (-LR 0.18)

Many PT’s look for negative findings during testing of Hoffman’s, Babinski, clonus and hyperreflexia to rule out myelopathy. However, these tests by themselves demonstrate low sensitivity and are not appropriate for ruling out myelopathy. The findings in this study are unique, as it is the first to identify a cluster of findings that not only function as a screening tool, useful for ruling out the condition of myelopathy, but also provide combinations that are confirmatory, ruling in conditions of myelopathy.
Cook C et al. Clustered clinical findings ifor diagnosis of cervical spine myelopathy. Journal of Manual and Manipulative Therapy Vol 18 No 4 2010
Traditionally, very little has been done in PT for cervical myelopathy management. In 2004, a case series was published (Browder et al. JOSPT), where mild cervical compressive myelopathy was treated with a combination of intermittent cervical traction and thoracic manipulation. All patients improved, although it was not quite clear if it was time, or the intervention that made the difference. However, this is a step in the right direction.

Neoplastic conditions

  • Age> 50 years

  • Previous history of cancer

  • Unexplained weightloss

  • Constant pain

  • Nightpain

Inflammatory or systemic disease

  • Temperature> 100 F

  • BP > 160/95 mmHg

  • Resting pulse >100

  • Resting respiration >25 bpm

  • Fatigue

Whiplash injuries

The whiplash can be either in flexion or extension. Not a diagnosis by itself. The hyperextension injury is the most disabling. Causes include MVA’s, sports injuries, direct trauma to head, neck or body, falls landing on head, trunk or shoulder. Likely lesions following a whiplash incident in the C spine include tears to the ligaments, muscles and discs, damage to the neurological, vestibular and vascular systems, occult fractures and facet joint injuries.

The main concern with treatment is with the recognition of severe damage, fractures or CNS involvement. The vertebral artery should not be tested for the first 4-6 weeks and therefore, no treatment that might threaten the artery should be given during this period.

In the early stage proceed carefully. Meadows advocates the use of a soft collar. This can be taken off when the capsular pattern disappears. This is usually after about 3 weeks. Once the capsular pattern is gone, and the vertebral artery tested, you can proceed with treating specific dysfunctions with more direct techniques.

You might consider delaying PT during the first 10 days to help settle down irritation in the CNS/sympathetic nervous system.
Whiplash recovery: 40% does well, 40% does moderately well, and 20% does poorly.
Ritchie et al. developed a whiplash clinical prediction rule to consolidate previously established prognostic factors for poor recovery from a whiplash injury. The CPR predicted 2 recovery pathways. Prognostic factors for full recovery were being less then 35 years of age and having an initial NDI score of <32%. Prognostic factors for ongoing moderate/severe pain and disability were being >35 years of age, having an initial NDI score >40%, and the presence of hyperarousal symptoms.
The median time for average person to get better is 31 days. Two percent is still disabled 1 year after injury. They present with varying degrees of pain, motion loss, headaches and emotional disturbances in the form of anxiety and depression. Management: adequate early pain management; specific rehab of motor deficits (non pain provoking); psychological intervention (decrease in psychological distress parallels decreasing pain and disability). A multidisciplinary approach seems warranted. In the presence of widespread mechanical and cold hyperalgesia, PT alone is insufficient. To reduce burnout and frustration, remember that much of the damage suffered is either irreversible or very slow to heal and essentially invulnerable to PT, at least directly.

  • Ritchie C, Hendrikz J, Jull G, El;iott J and Sterling M. (2015) External Validation of a clinical prediction rule to predict full recovery and ongoing moderate/severe disability following acute whiplash injury. Journal of Orthopedic and Sports Physical Therapy. Vol 45 No 4 242-251

  • Scientific monograph of the Quebec Task Force on whiplash-associated disorders: redefining “whiplash” and its management. Spine Vol. 20, No.8S, 1995

Cervical radiculopathy

Cervical radiculopathy is a disorder of the nerve root regardless of the cause (arthritic conditions, discogenic disorders, space occupying lesions, inflammation of the nerve root) Peak incidence is between the 4th and 5th decade. The C6-7 nerve root is most frequently involved. Ninety percent of the afflicted patients improve with conservative management. Twenty-six percent of those having surgery have a decline in status at one year follow up.

The following cluster of tests has been found to be most useful to identify cervical radiculopathy (Wainner et al. Spine 2003): ULTT +, cervical rotation to involved side< 60 degrees, Spurlings +, distraction relieves symptoms.

When two of these tests are positive there is a 21% probability of cervical radiculopathy.

Three positive tests: 65% probability, 4 positive tests: 90% probability.

Evidence for appropriate management is not great. A study by Cleland et al (JOSPT 2005) shows that a combined approach of cervical lateral glides, T spine manipulation, deep neck flexor strengthening and intermittent cervical traction is helpful. It showed that 91% of patients had decreased pain and improved function. A multimodal approach seems to work best.

Disc lesions

Posterolateral disc prolapses as they happen in the lumbar spine are relatively rare in the cervical spine. The nucleus takes up only 15% of the available space in the disc. According to Grieve it’s more common that nerve root irritation/compression is caused by spondylotic and arthritic changes. Disc prolapses causing root signs is usually limited to the lower cervical region due to the more developed uncinate processes higher in the spine. Flexion usually limited. At times there will be a torticollis. Pain is intense and may be scapular or radiating in the arm. Traction relieves symptoms. Compression, especially in flexion will reproduce local pain and likely peripheralization. X rays are usually negative.
Central herniation: over 45 years. Bilateral and upper extremity pain with multisegmental paresthesiae, especially in the hands, which is later felt in the feet as the condition progresses. Neck flexion reproduces paresthesiae. May cause cord compression and upper motor neuron signs. Traumatic posterior prolapse following MVA is probably a fairly common condition with as many as 25-40% of these patients showing evidence of one
Acute torticollis

Four known causes for acute torticollis:

  • Disc derangement. Patient usually wakes up in AM with deformity. Mobilization will worsen symptoms. Traction techniques with extension will help. Analogous to lateral shift in low back.

  • Facet joint dislocation

  • Spasm of sternocleidomastoid

  • Acute C2-7 facet joint impingement, with C2-3 being mostly affected, as this is a transitional vertebra. Mobilizations are highly effective.

Peripheral entrapment neuropathies of the UE

Ulnar Nerve

The ulnar nerve can get entrapped at the elbow at the cubital tunnel and at the wrist at Guyon’s canal.

Cubital tunnel syndrome is the second most common entrapment neuropathy in the UE.

The cubital tunnel is formed by the medial edge of the trochlea and olecranon laterally and the medial epicondyle medially. The ulnar collateral ligament forms the floor of the tunnel. The cubital tunnel retinaculum (or arcuate ligament) forms the roof. Flexion tightens the retinaculum, narrowing the tunnel. Overhead sports activities are a common source of ulnar nerve irritation. Repetitive activities may produce adaptive changes such as bony hypertrophy, extension restrictions, or valgus deformities. Instability of the ulnar nerve at the elbow can also cause neuropathy. It usually presents as aching pain over the medial side of the elbow, sometimes radiating to the hand. It also produces sensory disturbances (numbness, tingling, coldness) over the ulnar side of the hand and ulnar one and one-half digits. Popping or painful snapping of the nerve with flexion or extension can occur. Motor involvement affects the hand intrinsic musculature, but spares the flexor carpi ulnaris and flexor digitorum profundus.

Testing: sustained elbow flexion (1-3 minutes) will reproduce symptoms. Positive ANTT ulnar nerve.
Ulnar neuropathy in Guyon’s canal can be caused by carpal ganglions, hamate fractures, extrinsic trauma or compression. It may present as isolated or combined sensory and motor symptoms, depending on where the compression occurs. It can cause pain, paresthesia in the ulnar nerve distribution of the hand. Weakness may develop in the intrinsic muscles, producing decreased lateral pinch and grip strength. Patient may have problems with fine motor skills. Claw hand deformity may develop due to loss of intrinsic muscle strength.
Overt anesthesia along the arm cannot result from ulnar nerve compression. Medial arm symptoms arise from a site near, or proximal to, the axilla. Sensory innervation in the medial part of the arm comes from the medial brachial and medial antebrachial nerves from the medial cord.
To differentiate between C8-T1 radiculopathy and ulnar nerve entrapment, check strength of the extensor pollicis longus (EPL). The EPL is innervated by the radial nerve, level C8. Check sensation as well, as ulnar nerve sensory loss covers the medial hand and one and half fingers, whereas sensation loss in C8 dermatome is different.

Median nerve

The median nerve can get entrapped at the ligament of Struthers, the pronator teres, the site of branching of the anterior interosseous nerve and at the wrist.
Entrapment at the ligament of Struthers is rare, as this vestigial ligament is present in just 1% of the population. This ligament, if present, stretches between a humeral spur, 3-5 cm proximal to the elbow, and the medial epicondyle. It covers the median nerve.
The pronator syndrome mainly stems from 2 sites of compression:

  • A thickened lacertus fibrosis where it connects to the pronator teres muscle

  • Pronator teres hypertrophy or fibrous bands within the muscle

It presents as an insidious onset of proximal anterior forearm pain, with occasional hand pain. Repeated pronation and wrist flexion increases the pain. Night pain is uncommon. Resisted pronation and wrist flexion reproduces symptoms. Sensory symptoms may involve the radial hand and 3.5 digits. Motor involvement is less common. There may be soft tissue changes at the pronator teres. Positive adverse neural tissue tension for median nerve.
The anterior interosseous branch is susceptible to compression by fibrous bands from the deep head of the pronator teres or flexor digitorum superficialis muscles. The median nerve divides to form the anterior interosseous nerve at the distal edge of the pronator teres. Compression results from repetitive trauma, casts or contusions. The anterior interosseous syndrome presents as proximal forearm pain that is increased with activity. There are no sensory changes. There may be decreased dexterity or weakness in pinch grip.
Median nerve compression at the wrist (carpal tunnel syndrome) is the most common of all peripheral nerve entrapment syndromes. It may stem from any condition that decreases the size of the carpal tunnel: fluid retention, external compression, excessive callus formation or malalignment after a Colles fracture, lunate dislocation, ganglions and synovitis. It presents as an acute or insidious onset of pain, paresthesia or anesthesia over the radial side of the pal and radial three and one half digits. Pain may radiate proximal to the wrist and is often nocturnal. Weakness can occur in thenar musculature and 1st and 2nd lumbricals, which hinders opposition and precision maneuvers. There will be a positive Phalen’s test, positive ANTT for median nerve, volar swelling and thenar atrophy.
To differentiate between C6-7 radiculopathy and median peripheral nerve entrapment of the median nerve, check reflex and strength of brachioradialis. The brachioradialis is innervated by radial nerve, level C6. Check sensation as well, as median nerve sensory loss covers the first 3 fingers, whereas sensation loss in C6, 7 dermatomes is different.

Radial nerve

The radial nerve and its branches are vulnerable to compression from the mid humeral region to the wrist. External compression is common over the posterior humerus and at the wrist. Internal structures are more often at fault in the elbow and forearm, although direct trauma can injure the superficial radial nerve in the forearm.
High radial nerve palsy usually results from trauma such as fractures, tourniquet use and “Saturday night palsy”. Activities like wrestling, throwing, gymnastics and weightlifting can compress the radial nerve between triceps and humerus. It produces mixed motor and sensory symptoms. Depending on the level of the lesion it may or may not involve the triceps. Pain may radiate proximal or distal to the elbow. Sensory changes occur in the posterior forearm, dorsal hand and dorsal aspect of the radial 3 and one-half digits. Weakness may affect the supinator, wrist extensor, thumb extensor/abductor and finger MP extensor muscles.
Radial tunnel (or posterior interosseous) syndrome is the most common compression neuropathy of the radial nerve. The radial nerve splits near the radial head into the posterior interosseous and superficial radial nerves.

The posterior interosseous nerve (PIN) enters the 5 cm long radial tunnel, passing from the anterior to the dorsal compartment of the forearm. There are 4 common sites of compression in the radial tunnel:

  • Fibrous bands anterior to the radial head

  • A vascular arcade

  • The tendinous margin of the extensor carpi radialis brevis

  • The proximal edge of the supinator (arcade of Frohse)

The radial tunnel syndrome manifests as local tenderness and extensor weakness. Night pain is common. No sensory changes.
To differentiate between C6-7 radiculopathy and posterior interosseous nerve, check sensation as the PIN is a motor nerve only and provides no cutaneous sensation. The pain associated with PIN entrapment may simulate lateral epicondylitis, but careful palpation will give you the clue needed. The radial nerve will be tender on palpation.

ANTT is + for the radial nerve.


Goals of history taking

To determine the kind of disorder present. Is this patient an appropriate candidate for PT?

To determine whether there are any contra indications present to further physical examination and treatment techniques
To form a baseline against which progress can be measured
To obtain a detailed description of all patients symptoms
To obtain a chronological history:

  • of the present episode. Are symptoms static/worsening/improving? Has the patient had prior treatment, and if so what kind, and what were the effects?

  • of previous episodes

  • of related medical/family history

To make an assessment of:

  • the area/structure involved

  • the nature of the problem and the stage of the problem

  • the irritability of the condition

  • the behavior of symptoms

  • aggravating /easing factors

  • the patient as a person

  • the prognosis

Special questions:

  • Recent weight fluctuation? Reason?

  • Recent X rays? Results?

  • Medication for this and/or other conditions

  • Cardinal signs/symptoms

Systemic vs. musculoskeletal signs and symptoms
Clinical signs and symptoms of systemic pain

Recent, sudden

Does not present as a chronic problem


Knife like, stabbing, boring, deep, deep aching

Cutting, gnawing, throbbing

Bone pain

Related to the degree of noxious stimuli


Constant, no change, nightpain


Although constant, may come in waves

Gradually progressive


Symptoms not relieved by rest or change in positions
Aggravating factors:

Depends on the organ involved

Relieving factors:

Usually none, but also depends on the specific problem

Associated signs and symptoms:

Fever, chills

Unusual vital signs

GI symptoms (nausea, vomiting, anorexia, unexplained weight loss, diarrhea)

Painless weakness of muscles, more often proximal, but may occur distally

Excessive perspiration

Breathlessness at rest or after mild exertion

Bowel/bladder symptoms

Skin lesions, rashes or itches not related to musculoskeletal lesions

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