The loss of the facial identity through traumatic and dysmorphic factors (including the peripheral paresis of the facial nerve) is an intense psychotraumatical event associated with intense depression.

The evaluation of depression to 15 patients with hypertension and carotidian vascular changes revealed by echo-doppler associated with peripheral facial paresis therapeutically unsolved in 60 days, confirmed scores greater than 21 on Hamilton Scale (HDS). The study of the therapeutical means used in facial paresis treatment showed pharmacological type risk factors for depression (corticotherapy, antiinflamatory substances which conduct to ROS type reactions) and usual physio- and electotherapeutical techniques showed an increase of the iritative type potential on EEG standard examination.

The serotoninergical origin of the facial nerve, the high frequency of serotoninergic depression, the elevated scores on HDS justified the antidepressive serotoninergic activation treatment (escitalopram) combined with mimical facial training for 30 days with the following neurobiological action:

1. - at the amygdala level (emotional role acting and serotoninergic stimulation);

2. - at the amygdalian connections with the hippocampal zone and frontal cortex level;

3. - at the facial nerves neurons level through the reactivations of the serotoninergic input, deblocking of the ionic channels and the decrease of neuromotor inhibition.

The final evaluation demonstrated the significant amelioration of depression and an important remission of the facial motor deficit through mechanisms that suggested the potentiation of the serotoninergic action of antidepressive medication through the physical exercises and an secondary neuroprotection type effect at a hippocampal level.