can indeed serve as the necessary and su cient stimuli for chronic muscle length adaptation to adjust the basic muscle lengths.

In the normal situation it is not necessary to postulate that basic extraocular muscle lengths respond only to vergence stimulation and not to version stimulation. As both vergence stimulation and version stimulation occur, both could be slowly stimulating muscle length adaptation. However,the e ect of the version stimulation would average out to zero over time.The vergence stimulation,on the other hand, would exert a net e ect, changing the basic muscle lengths in the directions necessary to reduce the need for the vergence stimulation in the first place – a marvelous nega- tive-feedback servomechanism, as pointed out previously.

The mechanism just proposed would work in the normal situation, but there is strong evidence from what happens in strabismic states that extraocular muscle length adaptation responds to vergence stimulation primarily, and only minimally to version stimulation. And that is a fundamental di erence between extraocular muscles and the other skeletal muscles. The evidence is the same as that noted earlier simply the observation that chronic monocular deviations of the eyes, as in sensory exotropia or in esotropia with unilateral amblyopia, practically always become binocular deviations under anesthesia, with bilaterally abnormal basic muscle lengths.

The argument is this: In constant strabismic states where there is no fusion, there is no significant fusional vergence stimulation, but version stimulation still exists. If the extraocular muscles should adapt their lengths according to version stimulation, then the muscle lengths in the deviating eye in the patient with sensory exotropia would totally adapt to the deviated position.

The sound eye, spending its average time in straight ahead gaze, would have normal muscle lengths. However, this is clearly not the case, because in most cases of sensory exotropia, both eyes turn out under anesthesia, and in most cases of esotropia with unilateral amblyopia, the two eyes are essentially symmetric under anesthesia. By forced duction testing, especially in the cases of esotropia, the basic muscle lengths are clearly bilaterally abnormal.

The position of the eyes when asleep probably has little or no e ect on muscle length adaptation, because Breinin has shown that electrical activity in the extraocular muscles essentially disappears in deep sleep [24], and decreased stimulation of skeletal muscles significantly slows down muscle length adaptation, as shown by denervation experiments [19].

Figure 2.6 shows a patient illustrating the ine ectiveness of version stimulation. The muscle lengths clearly did not adapt to the positions in which the eyes were held by chronic everyday version stimulation.

Fig. 2.6 T hirty-three-year-old woman with esotropia since birth. Only her right eye was operated for the esotropia at the age of 2½ years. She has fixed with her LE only (top), as long as she can remember, because of mild hyperopia and amblyopia in her right eye. Neither eye has adapted to these positions, because when she is placed under deep anesthesia (bottom), both the eyes deviate rightward. The muscle lengths clearly did not adapt in response to chronic everyday version stimulation

Therefore we must conclude that the stimulation from vergence tonus is the primary regulator of extraocular muscle length adaptation, and that its e ects are bilateral. In this regard, the regulation of the extraocular muscle lengths appears to be fundamentally di erent from the regulation of the lengths of other skeletal muscles. Only the extraocular muscles experience this bilateral vergence stimulation. The other skeletal muscles receive primarily unilateral stimulation, or bilateral stimulation akin to version stimulation, and their lengths are responsive to these forms of stimulation as well as to stretching or slackening of the muscles depending on use.

2.2.6Evidence Against the “Final Common Pathway”

There is a potential problem with the conclusion that vergence tonus is the primary regulator of extraocular