Vascular Pathologies of the Neck

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Cervical arterial dysfunction (CAD) is an umbrella term used in manual therapy and physiotherapy to cover a range of vascular pathologies which may lead to cervico-cranial ischaemia. CAD is inclusive of all known vascular pathologies and anatomical structures that may be compromised by movement or manual therapy. Further, the clinical model of CAD incorporates the notion of assessing for patients presenting to physiotherapists with neuromusculoskeletal neck and head pain who may have an increased risk of developing an associated pathology. Thus the model has two dimensions: first, to identify underlying vascular pathologies masquerading as neuromusculoskeletal pain; second, to identify the risk of developing arterial pathology during assessment or intervention. The term was first described in 2008 (1) and has been adopted by the International Federation of Orthopaedic Manual Physical Therapists (IFOMPT) in their 2013 document: ‘International framework for examination of the cervical region for potential of Cervical Arterial Dysfunction prior to Orthopaedic Manual Therapy intervention’ (2)

The IFOMPT document provides clinical reasoning and physical examination guidance for clinicians and highlights the need for manual therapy clinicians to be cognisant with the concept and details of CAD. Much of the information on this page is detailed further in the IFOMPT document.

Note: The term should not be confused with cervical arterial dissection which is also referred to via the acronym CAD. This relates to a single, specific pathology (see below).

CAD itself is not a specific pathology diagnosis. Thus, there is a variation in clinical presentation which is dependent on the structure involved, the pathological mechanism and the stage at which the dysfunction presents. CAD is of relevance to clinicians due to the fact the pain is often an early presentation of many types of arterial dysfunction, Fig 1. Later ischaemic manifestations of CAD, such as cranial nerve dysfunction and brain ischemia, may be latent and develop hours, days or weeks after onset. Table 1 (below) details the range of presentations and associated clinical symptoms

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Clinically Relevant Anatomy

The contemporary approach to risk assessment of the cervical spine incorporates a ‘systems based approach’. This differs from previous paradigms by considering the complete intra and extra cranial arterial supply of the cervico-cranial region, and the wide range of associated pathologies. This includes the anterior cervical arterial system i.e. the common carotid artery (CCA) its related branches (internal and external) and pathologies, in addition to the previously considered posterior circulation, i.e. the vertebrobasilar arterial system (VBA).

Internal Carotid Artery

Knowledge of the anterior system is important for physiotherapists because:

1. The internal carotid artery (ICA) provides the most significant proportion of blood to the brain.
2. Pathological changes of the ICA are very common.
3. Blood flow in the ICA is known to be influenced by movement of the neck.
4. The ICA is commonly implicated in ischaemic stroke (see below ?link).

The two ICA’s carry around 80% of the blood flow to the brain compared to the 20% via the posterior system. It is primarily increased flow through the ICA and the presence of an intact circle of Willis, which helps maintain brain perfusion in the presence of vascular compromise in other parts of the system (i.e. vertebral arteries). Blood flow through the ICA is influenced by movement of the cervical spine i.e. primarily extension, and less so, rotation. To understand the relationship between the CA’s and stroke see http://www.youtube.com/watch?v=442s9a_TEL8

External Carotid Artery (ECA)

The ECA is a major artery of the cranio-cervical region. It arises from the common carotid artery at a bifurcation point around the C3 level (upper thyroid cartilage). It eventually forms the occipital artery and terminates in the maxillary artery and superficial temporal artery which may be implicated in cases of headache linked to temporal arteritis.

The vertebrobasilar arterial (VBA) system and vertebrobasilar insufficiency (VBI)

The VBA system supplies circulation to the hind-brain (i.e. brain-stem, medulla oblongata, pons, cerebellum, and vestibular apparatus). Entry to the skull is via the foramen magnum of the occiput. The vessels are ‘tethered’ at various points along the route:

• The C2 transverse foramina
• The C1 transverse foramina
• The atlanto-occiptal membrane.

It is this tethering, combined with the convoluted route of the vessels around C2/C1 and the occiput, which have been a cause of historical concern for manual therapists. Considering the anatomy of the upper cervical spine it is easy to appreciate how, during rotation, the contralateral vessel may be stretched, therefore potentially affecting flow (Fig. 2). Once inside the skull, the two vertebral arteries join each other to form the basilar artery, which in turn feeds into the circle of Willis. When there is a reduction of blood supply to specific parts of the hind-brain, certain signs and symptoms are displayed. This is what is referred to as VBI.

Mechanism of Injury / Pathological Process

Risk Factors

The following risk factors are associated with an increased risk of either internal carotid or vertebrobasilar arterial pathology and should be thoroughly assessed during the patient history:

• Past history of trauma to cervical spine / cervical vessels
• History of migraine-type headache
• Hypertension
• Hypercholesterolemia / hyperlipidemia
• Cardiac disease, vascular disease, previous cerebrovascular accident or transient ischaemic attack
• Diabetes mellitus
• Blood clotting disorders / alterations in blood properties (e.g. hyperhomocysteinemia)
• Anticoagulant therapy
• Long-term use of steroids
• History of smoking
• Recent infection
• Immediately post partum
• Trivial head or neck trauma
• Absence of a plausible mechanical explanation for the patient’s symptoms.

Clinical Presentation

• Head and neck pain
  
• 5D's And 3N's
  • Dizziness
  • Drop attacks
  • Diplopia
  • Dysarthria
  • Dysphagia
  • Ataxia
  • Anxiety
  • Nausea
  • Numbness
  • Nystagmus

Examination

The International Framework for Examination of the Cervical Region disucsses several techniques to assess for CAD:

• Blood Pressure
• Craniovertebral ligament testing
• Neurological examination
• Positional testing
• Palpation of the carotid artery

Importance of observation throughout history

Signs and symptoms of serious pathology and contraindications / precautions to treatment may manifest during the patient history stage of assessment. This is an opportunity to observe and recognise possible red flag indicators such as gait disturbances, subtle signs of disequilibrium, upper motor neuron signs, cranial nerve dysfunction, and behaviour suggestive of upper cervical instability (e.g. anxiety, supporting head/neck) early in the clinical encounter.

Differential Diagnosis

The following information is provided to assist in the differential diagnosis of musculoskeletal dysfunction from serious pathologies which commonly manifest as musculoskeletal dysfunction:

Differential diagnosis

	Internal carotid artery disease	Vertebrobasilar artery disease	Upper cervical instability
Early presentation	Mid-upper cervical pain, pain around ear and jaw (carotidynia), head pain (fronto-temporo-parietal); Ptosis; Lower cranial nerve dysfunction (VIII-XII); Acute onset of pain described as "unlike any other”.	Mid-upper cervical pain; occipital headache; Acute onset of pain described as "unlike any other”.	Neck and head pain; Feeling of instability; Cervical muscle hyperactivity; Constant support needed for head; Worsening symptoms.
Late presentation	Transient retinal dysfunction (scintillating scotoma, amaurosis fugax); Transient ischaemic attack; Cerebrovascular accident.	Hindbrain transient ischaemic attack (dizziness, diplopia, dysarthria, dysphagia, drop attacks, nausea, nystagmus, facial numbness, ataxia, vomiting, hoarseness, loss of short term memory, vagueness, hypotonia/limb weakness [arm or leg], anhidrosis [lack of facial sweating], hearing disturbances, malaise, perioral dysthaesia, photophobia, papillary changes, clumsiness and agitation); Cranial nerve dysfunction; Hindbrain stroke (e.g. Wallenberg’s syndrome, locked-in syndrome).	Bilateral foot and hand dysthaesia; Feeling of lump in throat; Metallic taste in mouth (VII); Arm and leg weakness; Lack of coordination bilaterally.

It is important to consider the above information in the context of the aforementioned risk factors.

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Management / Interventions

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Differential Diagnosis

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