PubMed1982
A new clinical case of Pontine Reticular Formation (P.R.F.) syndrome is reported and analysed using electro-oculograms. The CAT scan showed a probably metastatic tumour, clearly limited and located in the ventral part of the left tegmentum in the lower pons. The oculomotor disorders were typical of the P.R.F. syndrome and similar to those previously reported in pathological studies. The left P.R.F. damage was clinically evidenced by the loss of all leftward saccades (voluntary saccades and quick phases of nystagmus), including also those situated in the right hemifield of movement. It was noticed that the voluntary return movement driving both eyes from the right lateral position to the midline was remarkably slow and twice slower for the left eye (10 degrees/s) than for the right one (20 degrees/s). The loss of pursuit movements in the left hemifield of movement suggested that the lower part of the left P.R.F. was affected by the lesion. The preservation of normal leftward oculocephalic movements for the right eye indicated that the left abducens nucleus was spared. Lastly, the complete abductive paralysis of the left eye including the oculocephalic movement implied that the left abducens motoneurons passing through the lower part of the P.R.F. were damaged. All these functional and structural correlates are consistent with the location of the lesion given by the CAT scan. They are reviewed in the light of recent experimental and clinico-pathological data. A detailed physiopathological interpretation accounting for the slow voluntary movements, observed in place of the leftward return saccades in the right hemifield of movement, is proposed. The slowness of the movements of both eyes results from lack of phasic excitation of the motoneurons of the agonist muscles and from lack of phasic inhibition of the motoneurons of the antagonist muscles, both mechanisms being suppressed by the lesion which damages the excitatory burst neurons of the left P.R.F. As the tonic cells of the left P.R.F. are also out of action, these slow movements could mainly be controlled by the tonic cells of the right P.R.F. For the left eye, as the root fibres of the left abducens nucleus are damaged, no excitation can occur on the agonist muscle (left lateral rectus) and there is only a voluntary tonic disfacilitation of the motoneurons of the antagonist muscle (left medial rectus). For the right eye, the same mechanism involving the antagonist muscle (right lateral rectus) would be combined with some tonic excitation of the motoneurons of the agonist muscle (right medial rectus), thus accounting for the twice faster velocity of this eye. This tonic excitation reaching the right medial rectus could be mediated either by one of the other afferent neurons of the left abducens nucleus encoding eye position--namely those arising from the vestibular nuclei or from both prepositus hypoglossi nuclei--or by the right ascending tract of Deiters projecting to the right medial rectus motoneurons.