Abstract

Background and Goal of Study: We suggest the following pathogenesis of myoclonus in this case – variant of SPS in a vegetative state patients. Materials and Methods: Patient 22 years old drowned in water, was admitted to the ICU 3 months after hypoxia in vegetative state. Neurological symptoms were as follows: hyperkinesis (myoclonus with the rhythmic twitching of the hand, cranial muscles and total jerk of skeletal muscles at the end). MRI showed signs of diffuse atrophic changes of the brain and subcortical nuclei lesions (Fig 1). Proton MR spectroscopy found increase N-acetil aspartate at the subcortical nuclei, indicating a violation of their anatomical integrity against the background of repeated EEG monitoring of epileptic activity, bursts of typical myoclonus have not been identified, ie in this case, we observed EEG-negative form of myoclonus. Neuroimaging studies showed a fairly typical ischemia-hypoxic brain damage and subcortical nuclei lesions, but during positron emission tomography (PET) with fluorinedesoxiglucose, showed increased fixation of the radiopharmaceutical in the subcortical nuclei.Results: During therapy with clonazepam and zolpidem we observed a distinct positive effect - significantly diminished hyperkinesis, further spontaneous myoclonic hyperkinesis were not observed, one month after the patient began to fix a sight. Two months later the patient began to pronounce simple words. Conclusions and Discussion: Pharmacological inhibition of the activity of the SPS using drugs modulating the activity of GABA- system have reduced the number and severity of hyperkinesis, and expand the volume and the perception of sensory information by the brain, we observed the appearance of signs of consciousness in the form of short-term at first, then a more sustainable fixation of sight, transfer of a sight on demand.

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