Page 40 - BOAF Journal 1 2012:2707

Behavioral Optometry
BOAF
Volume1 Number1 2012
more often damage the path- ways of single or multiple EOM function. This commonly re- sults in limitations or loss of movement of muscles and re- sults binocularly in diplopia and confusion. An evaluation may reveal diplopia as the chief find- ing, however the more impor- tant consideration is the confu- sion that accompanies it. This condition makes it difficult for the patient to organize and move within their spatial world.
Patients with cortical le- sions should be evaluated by optometrists and recommenda- tions made as soon as possible. Typically rehabilitation thera- pists will provide orienting ac- tivities to help patients begin to expand their visual space on the side they are having diffi- culty with. The optometrist may also become involved and use their expertise to include guid- ance activities as well as prisms and lenses to help guide recov- ery. Often vestibular and cervi- cal input may be added to help guide and support the recovery process of gaze palsy and gaze preference.
Patients who suffer single and multiple EOM dysfunctions secondary to a paresis or palsy should also be evaluated and treated as soon as possible. Traditional treatment simply ad- dresses diplopia by covering the eye with the paresis or palsy. More advanced treat- ment plans are easily devised that should not only promote recovery, but also limit adapta- tions and control diplopia.
An example might be a left cranial nerve 6 paresis that lim- its abduction of the left eye. Traditional approaches would be to patch the left eye, limiting diplopia. This leads to a de- creased signal for abduction of the left eye that sets the stage for decreased EOM function and recovery. There is a greater chance for atrophy and muscle cell death of the left lateral rec- tus and contracture of the left medial rectus. This likely less- ens the chance of a full recov- ery both monocularly and bin- ocularly. A more advanced treatment plan would be to use either a right nasal sector oc- clusion or a binasal placed to limit diplopia from midline into left gaze. This also promotes direct and active use of the lat- eral rectus and decreases the opportunity for atrophy, muscle cell death and contracture of the medial rectus. Guyton found out that cell death in the EOM is common if movement has been limited. Probably just as important to the rehabilita- tion process is that this allows the left visual field to be used for orientation and mobility and lessening the chance of both walking into an object and a shift in the patients egocentric localization.
Posture and Mobility
One of the common overt observations of ABI is the chal- lenge to posture and mobility. An optometrist may look at mo- bility and observe the patient regarding motor performance
and visual scanning. It is im- portant to observe the location of the lesion, where they are looking and if they are walking straight or drifting to one side or not. A more in depth evaluation of mobility may include obser- vations of trunk, shoulders and hips during walking. Challenges in walking could be related to the input of a motor deficit, possible vestibular influence and the visual directing of mo- bility. The combination of the three inputs gives rise to one’s ability to egocentrically locate and guide mobility. One should be careful interpreting your test- ing and observations as they are also relative to differences in space. Performance may be different in a patient’s periper- sonal space (out to arms length) and extra-personal (beyond arm’s length). Thus testing at 16 inches for a visual midline may not be the same if the pa- tient is looking across the room during ambulation. Padula found that appropriate guid- ance, lenses, prisms, occlusion and visual rehabilitation might be used to help patients walk more appropriately and with less effort. One clinical pearl is to always consider trial framing any yoked prism before pre- scribing it for mobility.
Vestibular Dysfunction
Vestibular dysfunction is related directly to EOM function. This is because each semicircu- lar canal is neurologically con- nected to our eye muscles. Leigh and Zee present a nice
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