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Objective : To investigate cortical regions related to voluntary blinking. Methods : Transcranial magnetic stimulation (TMS) was applied to the facial motor cortex (M1) and the midline frontal region (Fz) in 10 healthy subjects with eyes opened and closed. Motor-evoked potentials were recorded from the orbicularis oculi (OOC), orbicularis oris (OOR), abductor digiti minimi and tibialis anterior using surface and needle electromyography electrodes. Facial M waves and blink reflex were measured using supramaximal electrical stimulation of the facial and supraorbital nerves. Results : TMS at Fz elicited 3 waves in OOC with no response in other tested muscles except for the early wave in OOR. Facial M1 stimulation produced only early and late waves. Because of their latencies, shapes, and relationship to coil position and stimulation intensity, early and late waves appeared to be analogous to the facial M wave and R1 component of the blink reflex. The intermediate wave at 6–8 ms latency was elicited in OOC by Fz stimulation with eyes closed. Conclusions : Since its latency matches the central conduction time of other cranial muscles and it has characteristic of muscle activation-related facilitation, the intermediate wave is presumably related to cortical stimulation. This result provides evidence that the cortical center for the upper facial movements, including blinking, is not principally located in the facial M1, but rather in the mesial frontal region.

Objective: The arterial concentration and the partial pressure of ammonia are elevated in patients with hepatic encephalopathy (HE). Postural instability is a possible symptom of HE. We investigated the relationship between the concentration/partial pressure of ammonia and postural control in patients with liver cirrhosis. Methods: 40 patients with cirrhosis of various etiologies (alcoholic: 21, viral: 14, other: 5) and Child-Pugh-Stages (A: 17, B: 11, C: 12) were tested for postural control using posturography, an objective method to quantify postural sway (Smart EquiTest, NeuroCom International) and compared to 15 healthy controls. Arterial ammonia concentrations and pH were measured and the partial pressure of ammonia calculated by standard methodology. Patients underwent neurological examination to exclude other causes for postural instability. Reitan A test was used to diagnose hepatic encephalopathy. Results: Patients with liver cirrhosis showed an impaired postural control compared to healthy controls. (Mann-Whitney U test: p = 0.001) The patients with encephalopathy (Reitan A > 60 sec) performed significantly worse in posturography than those without encephalopathy (Reitan A < 60 sec). (p = 0.004) In patients with impairment of postural control the concentrations (p = 0.03) and partial pressure (p = 0.01) of ammonia were significantly higher than in those without postural instability. The concentration/partial pressure of ammonia also correlated with the severity of liver disease (Child-Pugh-Stage: p = 0.02), (Child-Pugh-Score: Spearman R = 0.5; p = 0.0003) and performance on Reitan A test (Mann-Whitney U test: p = 0.005/0.006). Conclusion: The significant correlation of the arterial concentration/partial pressure of ammonia with postural control in patients with liver cirrhosis confirms that postural instability is part of the nenrologic alterations of hepatic encephalopathy.