Modulation of oscillatory alpha activity in the somatosensory system by attention and hepatic encephalopathy

3 in particular alpha activity in this context has not yet been studied. In a second study, patients with liver cirrhosis and varying degrees of HE and healthy control subjects received electrical stimulation of sensory fibers of the right median nerve. The stimulus-induced rebound of alpha activity within the primary somatosensory cortex (S1) contralateral to the stimulated hand significantly differed between patients with manifest HE and controls. Increasing HE disease severity as quantified by the CFF was associated with a decreased peak frequency of S1 alpha activity and a delayed alpha rebound. The slowed frequency substantiates a global slowing of oscillatory brain activity as a key pathophysiological mechanism in HE. The delayed alpha rebound presumably indicates an impaired, slowed capability of the somatosensory system to adjust activation levels back to the default state. In conclusion, this thesis extends the understanding of the functional role of oscillatory alpha activity in the healthy and pathologically impaired brain. By demonstrating its use as a sensory gating mechanism during the perception of pain, these findings might contribute to the development of new methods of pain relief and treatment. In addition, alterations of somatosensory alpha activity in association with HE as an example of pathologically impaired brain function were identified. These alterations broaden the understanding of the pathophysiological mechanisms of HE and might provide new parameters for an early diagnosis of the disease.