a 49-year - old man with a history of sick sinus syndrome presented with quadriplegia and ophthalmoplegia .
brain magnetic resonance imaging ( mri ) and an angiography examination , which were performed a day after quadriplegia , revealed acute brain infarction in the bilateral midbrain , right median thalamus , and superior cerebellum associated with the distal basilar artery occlusion .
it is also unclear whether the mechanism of symptomatic bruxism is identical with that of idiopathic sleep bruxism .
it has been shown that rhythmic jaw movement is generated by a neuronal activation in the brainstem of animals.7 rhythmic firing of interneurons in the pontine reticular formation ( prf ) and a connection between the oral motor nuclei and the prf have been observed.7 - 10 rodents move their jaws continuously and cows ruminate throughout the day .
however , the activity of the generator is so weak that the release from high cortical inhibition during normal sleep may not be sufficient to cause bruxism . thus , the release phenomenon due to sleep and other factors such as dental problems , smoking , alcohol , and the coma state6 may cause bruxism . in our case ,
bilateral midbrain infarction may have caused the interruption of higher cortical inhibition and damaged the dentato - rubro - olivary pathway .
although higher cortical inhibition is interrupted , the brainstem generator may not be sufficient to cause bruxism .
additional damage to the dentato - rubro - olivary pathway may cause bilateral olivary hypertrophy , which can stimulate the prf . because no connection between the oral motor nuclei and the inferior olivary nuclei has been observed in animal study
, we do not think that the hypertrophied olivary nucleus directly stimulates the motor nucleus in the brainstem.8 instead , hyperactive bilateral prfs may cause bruxism . pollack and cwik have reported bruxism after cerebellar hemorrhage,5 which may also be related to the damage to the dentato - rubro - olivary pathway .
unlike palatal myoclonus , bruxism requires bilateral harmonic rhythmic contraction and relaxation of involved muscles . since the neurons in the prf project to both the trigeminal motor nuclei,8 the prf may induce the contraction of one side and relaxation of the opposite side . on the other hand , the normal side can influence both
we suspect that this is a reason why bruxism is very rare in patients with brainstem infraction . in conclusion ,
furthermore , we suggest that the human bruxism generator may be located in the prf .
large bilateral midbrain lesions that interrupt cortical inhibition seem to produce bilateral olivary hypertrophy , resulting in bruxism in the presence of the intact pontine generator .
 delayed - onset continuous bruxism due to brain stem infarction has not yet been reported . a 49-year old man presented with quadriplegia and ophthalmoplegia . 
 brain mri showed acute infarction in the bilateral midbrain , right thalamus and the superior cerebellum . 
 one month later , the patient developed bruxism which persisted during sleep . a palatal myoclonus was not observed . 
 follow up mri taken 4 months later showed bilateral olivary hypertrophy . 
 we suggest that the patient 's bruxism may be related to the olivary hypertrophy . 
 the bruxism generator may be located in the pontine - reticular - formation ( prf ) . 
 bilateral large midbrain lesions interrupting the cortical inhibition may have produced bilateral olivary hypertrophy , which could stimulate the prf , producing continuous bruxism . 
CASE REPORT
DISCUSSION