Section 5: Physical examination

International Framework for Examination of the Cervical Region

Blood pressure[edit | edit source]

Hypertension is considered a risk factor for carotid and vertebral artery disease. More acutely, an increase in blood pressure may be related to acute arterial trauma, including of the internal carotid and vertebral arteries[1]. Evaluation of blood pressure as part of the physical examination may therefore be a valuable test to inform clinical reasoning.

Resting blood pressure should be taken in either sitting or lying, with the arm (brachial pulse site) being at the same level (in relation to gravity) as the heart / 4th intercostal space. A validated monitoring unit should be used ensuring the correct cuff-size. The cuff should be fitted so that two adult fingers can be inserted at the top and bottom when deflated. The patient should remain static in a calm environment for at least five minutes prior to testing. Repeat measurements can be taken leaving two minutes between each measurement.

Normotensive range (non-diabetic adult) is systolic 120-140mmHg / 70-90mmHg diastolic[2].

Although hypertension is an undoubted strong predictor of cardiovascular disease, interpretation of readings must be in the context of other findings, and sound clinical reasoning. Vascular disease is an interplay between various factors, of which high blood pressure is just one (albeit a consistently important one). Blood pressure is a graduated, continuous measure and as such cannot have a threshold. The physical therapist should keep these points in mind during clinical decision-making. Hypertension and neck pain are only two of the many factors which influence the decision on probability of vascular pathology. Data regarding scaled risk is equally as clinically useful. There is a positive correlation between increased systolic and diastolic pressure and risk of stroke, which is the higher the pressure, the greater the risk. This would mean that a patient with say 190mmHg / 100mmHg is at greater risk than a patient with 160mmHg / 95mmHg. Thus, the risk is different even though they are both hypertensive. However, to reiterate, the actual utility of these data in isolation is limited as the true clinical risk is dependent on additional co-existing factors[3].

Patients with hypertension that has not been previously identified should be advised to discuss its implications with their primary care provider.

Craniovertebral ligament testing[edit | edit source]

Instability of the craniovertebral ligaments could compromise the vascular and neurological structures in the upper cervical region. Mechanisms for causing symptoms and signs include: C1-C2 instability causing abnormal pressure on cervical nerves, vertebral artery compromise[4][5], and cord compression[6][7]. Whether to test for instability is therefore an important decision when suspecting CAD. The presence of instability is a clear contraindication to the use of OMT techniques[8].

There are a variety of ligaments that act together to maintain stability, and yet allow flexibility of the cervical region. These include the anterior and posterior longitudinal, interspinous, intertransverse, tectorial membrane, alar, transverse and ligamentum flavum ligaments[9].

Symptoms and signs of instability include[10]:

  1. Facial paraesthesia secondary to dysfunction of the connections of the hypoglossal nerve, as well as the ventral ramus (neck-tongue paraesthesia) and the dorsal ramus (facial numbness) of C2
  2. Drop attacks
  3. Bilateral or quadrilateral paraesthesia or motor deficits including weakness / incoordination
  4. Nystagmus
  5. Nausea.

Traditional instability testing techniques of the cervical region included the Sharp-Purser test, which is a comparatively safe procedure to perform to test the excursion of movement when relocating the dens to the atlas, in order to assess the transverse ligament. Other assessment procedures for instability included the tectorial membrane distraction and the alar ligament side flexion/bending and rotation tests[11][10]. However in recent times, assessment of ligament stability has moved to systematically working through a series of active / patient generated, passive / therapist generated (with overpressure), and passive accessory movement tests, in order to feel the degree of movement or restriction at each joint and therefore ligament integrity, as well as to reproduce the patient’s symptoms.

Examples of active / patient generated tests for assessing cervical ligament integrity include:

  • Atlanto-occipital joint isolation (nod)
  • C1-C2 rotation with the neck flexed
  • C2-C3 rotation with protraction and retraction
  • Upper cervical extension, and rotation and lateral flexion to same side (C0-C3)

Examples of passive / therapist generated (with overpressure) tests for assessing cervical ligament integrity include:

  • Fixation of C1 via the transverse processes of C1 and passive flexion/extension of the occiput (C0-C1)
  • Fixation of the C2 spinous process with passive side bending or rotation of the occiput (C0-C2)

Examples of accessory movement tests for assessing cervical ligament integrity include[10]:

  • Transverse atlantal ligament stress test (modified Sharp-Purser test)
  • Alar ligament test.

(A useful resource for description of these tests is Mintken et al[12], which includes reference to videos that are available online).

Signs of instability from the aforementioned tests may include:

  1. Increase in motion or empty end-feel
  2. Reproduction of symptoms of instability
  3. Production of lateral nystagmus and nausea.

For each individual patient, a decision needs to be made regarding the value of performing any craniovertebral ligament tests, evaluating the risks and benefits of any specific test procedure using current evidence from research investigating validity of testing (e.g.[13]). However, the evidence of the predictive ability of these tests to identify instability is lacking and the physical therapist should carefully consider whether physical testing is prudent or safe in the presence of subjective symptoms of instability. In some situations, for example a post acute trauma presentation following a road traffic accident, the best decision would be to support them with a cervical collar pending radiological investigation.

Patients who have age-related loss of spinal movement, or have experienced cervical region trauma (e.g. whiplash), or who have pathological conditions (congenital e.g. Downs syndrome, inflammatory e.g. rheumatoid arthritis, or marked degeneration e.g. osteoarthritis) that may affect cervical spine ligament integrity require further craniovertebral ligament screening e.g. flexion-extension radiographic views and / or MRI.

Neurological examination[edit | edit source]

Examination of the peripheral nerves, cranial nerves, and for an Upper Motor Neurone lesion will assist in evaluating the potential for neuro-vascular conditions [see Fuller (2008)[14] for a detailed description of how to perform testing or Blumenfeld (2010)[15]].

Positional testing[edit | edit source]

Provocative positional testing is frequently used in practice. It is intended to provide a challenge to the vascular supply to the brain, and the presence of signs or symptoms of cerebrovascular ischaemia during or immediately post testing is interpreted as a positive test. Sustained end-range rotation has been advocated, and has been described as the most provocative and reliable test[16]. The sustained pre-manipulative test position has also been advocated[17]. However, the predictive ability of either of these tests to identify at risk individuals is lacking.

Palpation of the carotid artery[edit | edit source]

Palpation of the common and internal carotid arteries is possible due to the size of these vessels and their relatively superficial anatomy. Although no meaningful diagnostic utility statistics exist in relation to its precise role in predicting potentially adverse outcomes, carotid palpation is conventionally used as part of a clinical work-up for carotid artery dysfunction (e.g.[18][19][20]). Asymmetry between left and right vessels is assessed, and a pulsatile, expandable mass is typical of arterial aneurysm. Such a finding should be considered in the context of other clinical findings. It is possible for dissections and disease of the carotid arteries to exist in the absence of aneurysm formation, therefore a negative finding should not be used to refute the hypothesis of arterial dysfunction.

Palpation of the vertebral arteries is much less likely to provide meaningful information due to the small diameter of the vessel and its relatively inaccessible anatomy.

As pulse palpation is a relatively simple psycho-motor skill, training in this area should be focused on anatomical landmarks and vessel palpation. Ideally, the physical therapist would aim to understand and experience both normal and pathological pulse quality.

Differentiation[edit | edit source]

Differentiation of a patient’s symptoms originating from a vasculogenic cause with complete certainty is not currently possible from the physical examination. Thus, it is important for the physical therapist to understand that headache / neck pain may be the early presentation of an underlying vascular pathology[21][22]. The task for the therapist is to differentiate the symptoms by:

  1. Having a high index of suspicion
  2. Testing the vascular hypothesis.

This process of differentiation should take place from an early point in the assessment process i.e. early in the patient history. The symptomology and history of a patient experiencing vascular pathology is what may alert the physical therapist to such an underlying problem[21][22]. A high index of suspicion of cervical vascular involvement is required in cases of acute onset neck/head pain described as “unlike any other”[22]. Physical therapists may be exposed to patients presenting with the early signs of stroke (for example, neck pain / headache) and as such need both knowledge and awareness of the mechanisms involved. A basic understanding of vascular anatomy, haemodynamics and the pathogenesis of arterial dysfunction may help the physical therapist differentiate vascular head and neck pain from a musculoskeletal cause[21][22] through interpretation of the patient history data and tests in the physical examination. Kerry and Taylor[23] provide a summary of key physical examination tests and their value for differentiating vasculogenic head and neck pain, including: cervical rotation positional test, cervical extension positional test, blood pressure examination, cranial nerve examination, eye examination, use of hand held Doppler ultrasound, holding head and turning body test, and the Dix-Hallpike manoeuvre.

Refer on for further investigation[edit | edit source]

There are no standardised clinical guidelines for medical diagnostic work-up in respect to vertebral and carotid arterial dysfunction. It is recommended that the physical therapist follows local policy in referring for further investigation. Conventionally, duplex ultrasound, magnetic resonance imaging/arteriography, and computed tomography are used in the work-up[19][24]. Being non-invasive and cheaper, duplex ultrasound is often considered first. The primary aim is to differentiate between haemorrhagic sources for the signs and symptoms and any other cause, as this will dictate the management pathway. It is recommended that physical therapists refer for immediate medical investigation when their clinical suspicion is supported by the reasoned historical details and clinical examination findings as suggested in this document.

Additional training[edit | edit source]

It is acknowledged that some physical tests included in this section may not be in the domain of current OMT practice in some countries. It is recommended that in those countries where these tests are not within the domain of current practice that their use is considered. Any additional training required in physical examination techniques could be achieved within a physical therapist’s local environment.

References[edit | edit source]

  1. Arnold M, Bousser G, Fahrni G, et al (2006). Vertebral Artery Dissection Presenting Findings and Predictors of Outcome. Stroke 37:2499-2503.
  2. Mancia G, De Backer G, Dominiczak A et al (2007). Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Journal of Hypertension 25(6):1105-87.
  3. Nash I (2007). Reassessing normal blood pressure: Blood pressure should be evaluated and treated in the context of overall cardiovascular risk. British Medical Journal 335:408-9.
  4. Savitz S, Caplan L (2005). Vertebrobasilar Disease. The New England Journal of Medicine 352:2618-2626.
  5. Thanvi B, Munshi SK, Dawson SL, et al (2005). Carotid and vertebral artery dissection syndromes. Postgraduate Medical Journal 81(956):383-8.
  6. Bernhardt M, Hyess RA, Blume HW, et al (1993). Cervical spondylotic myelopathy. The Journal of Bone and Joint Surgery American 75:119-128.
  7. Rao R (2002). Neck pain, cervical radiculopathy, and cervical myelopathy. The Journal of Bone and Joint Surgery 84A(10):1872-1881.
  8. Gibbons P, Tehan P (2006). HVLA thrust techniques: What are the risks? International Journal of Oestopathic Medicine 9(1):4-12.
  9. Panjabi MM, White AA (1990). Physical properties and functional biomechanics of the spine. In: Clinical Biomechanics of the Spine, 2nd edn, Chapter 1. Philadelphia, J. B. Lippincott. P33.fckLR1990.
  10. 10.0 10.1 10.2 Gibbons P, Tehan P (2005). Manipulation Of The Spine, Thorax And Pelvis: An Osteopathic Perspective, 2nd Edn, Churchill Livingstone.
  11. Cattrysse E, Swinkels R, Oostendorp R, et al (1997). Upper cervical instability: are clinical tests reliable? Manual Therapy 2(2):91-97.
  12. Mintken PE, Metrick L, Flynn TW (2008a). Upper cervical ligament testing in a patient with os odontoideum presenting with headaches. J Orthop Sports Phys Ther 38(8):465-475.
  13. Kaale BR, Krakenes J, Albrektsen G, et al (2008). Clinical assessment techniques for detecting ligament and membrane injuries in the upper cervical spine region: a comparison with MRI results. Manual Therapy 13(5):397-403.
  14. Fuller G (2008). Neurological examination made easy. 4th Edition, Elsevier.
  15. Blumenfeld H (2010). Neuroanatomy through Clinical Cases. 2nd Ed. Available at: http://www.neuroexam.com/ Accessed January 2013
  16. Mitchell J, Keene D, Dyson C, et al (2004). Is cervical spine rotation, as used in the standard vertebrobasilar insufficiency test, associated with a measureable change in intracranial vertebral artery blood flow? Manual Therapy 9(4):220-7.
  17. Rivett DA, Shirley D, Magarey M, et al (2006). Clinical Guidelines for Assessing Vertebrobasilar Insufficiency in the Management of Cervical Spine Disorders. Australian Physiotherapy Association: Melbourne.
  18. Cournot M, Boccalon H, Cambou JP, et al (2007). Accuracy of the screening physical examination to identify subclinical atherosclerosis and peripheral arterial disease in asymptomatic subjects. Journal of Vascular Surgery 46(6):1215-21.
  19. 19.0 19.1 Cury M, Greenberg RK, Morales JP, et al (2009). Supra-aortic vessels aneurysms: diagnosis and prompt intervention. Journal of Vascular Surgery 49:4-10.
  20. Atallah PC, Atallah P, Kashyap V (2010). Internal carotid artery aneurysm discovered by palpation of asymmetric pulses. The American Journal of Medicine 123(7):e1-e2.
  21. 21.0 21.1 21.2 Rivett DA (2004). Adverse effects of cervical manipulative therapy. In J.D. Boyling and G.A. Jull (eds.), Grieve’s Modern Manual Therapy of the Vertebral Column (3rd ed). Churchill Livingstone: Edinburgh 533-549.
  22. 22.0 22.1 22.2 22.3 Taylor AJ, Kerry R (2010). A ‘system based’ approach to risk assessment of the cervical spine prior to manual therapy. International Journal of Osteopathic Medicine 13:85-93
  23. Kerry R, Taylor AJ (2006). Cervical arterial dysfunction assessment and manual therapy. Manual Therapy 11(3):243-253.
  24. Jones WT, Pratt J, Connaughton J et al (2010). Management of a nontraumatic extracranial internal carotid aneurysm with external carotid transposition. Journal of Vascular Surgery 51:465–467