Relatively recently, the Sharp-Purser test has become in vogue. The test was originally designed to test sagittal stability of the atlanto-axial segment in rheumatoid arthritic patients. In these patients, a number of pathological conditions can affect the stability of the osseoligamentous ring of the median joints of the atlanto-axial segment. The articular cartilage between the odontoid and the anterior arch of atlas can degenerate and thin, the dens can become softened, the ligament's collagen affected so that it becomes lax and there can even be ossification of the ligament.

The aim of the test is to determine whether the patient's central nervous system's signs and/or symptoms are being caused by such an instability. The purpose of this article is to review the relevant anatomy and pathomechanics, the test itself, its results and the interpretation of such results. In addition, an opinion will be offered as to the value of the test based on its strengths and weakness' and potential hazards.

Anatomy and Biomechanics

The dens, anterior arch of atlas and the transverse ligament are the primary anteroposterior stabilizers of the atlantoaxial segment with the alar ligaments acting as secondary restraints. The principle role of the ligament is to prevent the atlas from translating anteriorly on the axis during flexion and so compromising the spinal cord, medulla, vertebral arteries, superior sympathetic ganglion and nasopharyn. Normally, the transverse ligament limits translation in adults to about 3 millimeters and in children to about 8 millimeters. However, in posttraumatic or rheumatoid laxity these values can be dramatically exceeded. Generally adult translational values in excess of 4 millimeters are considered as prime candidates for surgery especially if they are type 1 tears (ligament substance). The structures that may be compromised include the upper spinal cord, the medulla, the vertebral arteries, the superior sympathetic ganglia positioned over the anterolateral aspects of the axis and the nasopharynx sitting anterior to the anterior tubercle of the atlas.

From the anatomy, it is reasonable to assume that symptoms that may be provoked from compression of these structures may include:

• bilateral or quadrilateral parasthesia (spinal cord, vertebral arteries)
• hemiparasthesia (vertebral artery ((Wallenberg's syndrome))
• hemi-facial parasthesia (vertebral artery ((Wallenberg's syndrome))
• tongue numbness (vertebral artery)
• type 1 dizziness (vertebral artery, cranial nerve 8)
• type 2 dizziness (superior cervical ganglion, cranial nerve 10, arthrogenic)
• nystagmus (vertebral artery, cranial nerve 8)
• nausea (vertebral artery, superior cervical ganglion, cranial nerve 10 and 8, arthrogenic)
• pupil dilation or constriction (vertebral arteries, superior cervical ganglion)
• dysphagia, gaging, reflex swallow (retropharyngeal hematoma, nasopharyngeal compression)
• dysarthria (cranial nerves 9 and 12)
• dysphasia (vertebral artery)
• dysphonia (cranial nerve 10 and 11)
• drop attack (vertebral artery, cranial nerve 8)

With the exception of the type 1 and 2 dizziness and the tongue numbness, all of the other signs and/or symptoms must be considered cardinal in the light of their onset with head positioning. The purpose of the Sharp-Purser test is to differentiate the cause of these cardinal signs and symptoms.

The Sharp-Purser Test

The patient is asked to flex the head and relate to the examiner any signs or symptoms that this might evoke. Local symptoms such as soreness etc. are ignored for the purposes of evaluating the test. If no cardinal symptoms are provoked, the test is discontinued. However, if cardinal symptoms are provoked a provisional assumption is made that they are caused by excessive translation of the atlas compromising one or more of the sensitive structures listed above. The assumption is tested when the examiner employs one of two methods of reducing the potential anterior translation. With the flexed position maintained, either the forehead can be stabilized and the axis manually translated anteriorly, or the axis can be stabilized and the head translated posteriorly with pressure against the forehead. In either case, the segmental effect is the same, The dens is either relatively or actually moved anteriorly out of the spinal canal. If the anterior excessive translation is in fact the cause of the cardinal signs or symptoms and if the Sharp-Purser maneuver has managed to reduce the translation, the signs and symptoms will disappear thereby proving that the sagittal instability of the atlanto-axial complex is the cause.

Discussion

Among the problems with the test are the following:

As the provocation of cardinal symptoms with neck flexion is a rare event, the average therapist will not be practised with finding the appropriate landmarks and a delay will occur in correcting the adverse condition. This will cause undue strain to be imparted to an already damaged ligament which may just be holding on.

The symptoms may be originating from a structure other than the spinal cord. An example here would be the Arnold-Chiari malformation a congenital anomaly that includes a hind brain arteriovenous fistulae and a cerebellum that is elongated sometimes extended into the spinal canal. While this may remain stable in the adult, the effect of trauma may cause some bleeding and thrombus formation in the affected vessels. Prolongation of neck flexion as the symptoms are produced while the examiner finds the axis and carries out the test may conceivably produce irreversible and serious consequences. We have little if any idea of what prolonged neck flexion may do to this mass of abnormal blood vessels.

The test was designed for rheumatoid arthritic patients and its sensitivity on post-traumatic patients has not be evaluated. In addition, there are added complications in the traumatic lesion that are not present in the arthritic. Even apart from the fact that type 1 tears are less common than type 2 (avulsion fractures), a large proportion of transverse ligament tears are associated with overt fractures and unfortunately, almost 30% of cervical fractures are missed radiographically. While we think we have some knowledge of the mechanics of the craniovertebral segments even in the face of ligamentous insufficiency, do we really understand what sustained fracture will do to a fracture of the atlas or dens.

If the symptoms are arising from compression of a compromised vertebral artery then even short duration sustainment of the flexed position may be dangerous. While we believe we understand what positions that occlude the artery, do we aware of the positions that will adversely stress a pseudoaneurysm, an intimal tear or thrombus formation.

While all of the above consider risk, we must also ask ourselves what do we get from the test. Do we really need to differentiate the sources of cardinal signs and symptoms related to head position. Does it really matter if they are being caused by the lower or upper cervical segments, will it change our management of the patient if we can determine the level that is compressing the cord or vertebral artery. If for example neck flexion provokes parasthesia in the arms and legs consider the following three scenarios. One, flexion produces it, you as the therapist will return the patient to the physician. Two, flexion produces it and the Sharp-Purser test fails to relieve it, you return it to the physician. Three, flexion produces the symptoms and the test relieves them, you send it back to the physician. In all cases, the patient should be returned to the physician because there is not a single benign cause for these symptoms that can be assumed until more objective testing has been carried out regardless of the outcome of the test. So, if the same action results whether the test is carried out or not and if carried out, what the result is, why bother doing the test, especially as there is an apparent risk to it.

Finally, more objective testing such as MRI or CT scanning or even flexion/extension radiography will provide a more definitive diagnosis more safely.

In conclusion, I would suggest that this test is not without its risks. It seems reasonable that any patient in whom a head position provokes cardinal signs or symptoms should immediately be moved out of that position to relieve the stress causing said signs and symptoms. This is not the time to practice your surface anatomy especially when you may be a little flustered by the patient telling you that all four limbs are tingling, he has tunnel vision, or that his lips are tingling. A better approach would be a comprehensive neurological examination that includes cranial nerve and long tract testing and taking a good history that would look for indications of neurological or neurovascular compromise, congenital anomalies and fractures. Just because we have a test for a thing, it does not mean that we have to do it.