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An experimental study was proposed, with the consent of the patient, in which an attempt was made to pharmacologically uncouple the brainstem neuronal activity from the cortical one. Simultaneously with the pharmacological uncoupling, the EMG activity with a coaxial needle on the left masseter was monitored and contextually the blink reflex. The experimental model, which we are going to explain briefly, was created through two essential elements, namely: the choice of the specific anesthetic for the purpose of the study (propofol) and the control of the electrophysiological activity of the brainstem through the blink reflex | An experimental study was proposed, with the consent of the patient, in which an attempt was made to pharmacologically uncouple the brainstem neuronal activity from the cortical one. Simultaneously with the pharmacological uncoupling, the EMG activity with a coaxial needle on the left masseter was monitored and contextually the blink reflex. The experimental model, which we are going to explain briefly, was created through two essential elements, namely: the choice of the specific anesthetic for the purpose of the study (propofol) and the control of the electrophysiological activity of the brainstem through the blink reflex | ||
===== | ===== Propofol ===== | ||
The effects of anesthetics produce loss of consciousness, memory, changes in spontaneous activity, attenuation of protective reflexes, loss of postural reflexes and also adverse effects such as hallucinations, euphoria and amnesia. Furthermore they may affect the level or homeostasis of neurotransmitters in the brain such as dopamine, noraepinephrine and acetylcholine (ACh).<ref>Angel A. : Central neuronal pathways and the process of anaesthesia. British Journal of Anaesthesia 1993; 71:148-163</ref> Ach was the first neurotransmitter to be described and cholinergic neurons are widely distributed in the brain. Cholinergic mechanisms are known to be important in the striatum where a balance between dopamine and ACh release ensures normal motor output,<ref>Iversen SD.: Behavioural evaluation of cholinergic drug. Life Sciences 1997; 60: 1145-1152</ref> hippocampus and frontal cortex where ACh plays an important role in the regulation of consciousness, memory etc. | The effects of anesthetics produce loss of consciousness, memory, changes in spontaneous activity, attenuation of protective reflexes, loss of postural reflexes and also adverse effects such as hallucinations, euphoria and amnesia. Furthermore they may affect the level or homeostasis of neurotransmitters in the brain such as dopamine, noraepinephrine and acetylcholine (ACh).<ref>Angel A. : Central neuronal pathways and the process of anaesthesia. British Journal of Anaesthesia 1993; 71:148-163</ref> Ach was the first neurotransmitter to be described and cholinergic neurons are widely distributed in the brain. Cholinergic mechanisms are known to be important in the striatum where a balance between dopamine and ACh release ensures normal motor output,<ref>Iversen SD.: Behavioural evaluation of cholinergic drug. Life Sciences 1997; 60: 1145-1152</ref> hippocampus and frontal cortex where ACh plays an important role in the regulation of consciousness, memory etc. | ||
Propofol is thought to potentiate the inhibitory effect of GABAA receptors and to have a different action from barbiturates or benzodiazepines. An elegant study<ref>Kikuchi T, Wang Y, Sato K, Okumura F.: In vivo effects of propofol on aceylcholine release from the fronatl cortex, hippocampus and striatum studied by intracerebral microdialysis in freely moving rats</ref> carried out through intracerebral microdialysis in mice demonstrated that propofol, with doses of 50 mg/kg, decreased the release of ACh from the frontal cortex by 85%, by 72% by the hippocampus and by 19% by the striatum. | Propofol is thought to potentiate the inhibitory effect of GABAA receptors and to have a different action from barbiturates or benzodiazepines. An elegant study<ref>Kikuchi T, Wang Y, Sato K, Okumura F.: In vivo effects of propofol on aceylcholine release from the fronatl cortex, hippocampus and striatum studied by intracerebral microdialysis in freely moving rats</ref> carried out through intracerebral microdialysis in mice demonstrated that propofol, with doses of 50 mg/kg, decreased the release of ACh from the frontal cortex by 85%, by 72% by the hippocampus and by 19% by the striatum. | ||
===== | ===== Blink reflex ===== | ||
The blink is a reflex that is evoked by hitting the eyebrow region on one side of the forehead. Electrophysiologically it is possible to evoke it by applying an electrical stimulus on the eyebrow arch in correspondence with the supraorbital foramen. The responses are recorded through two surface electrodes positioned on the orbicularis oculi muscle on each side and the motor potentials can be mainly represented by two events, namely the ipsilateral R1 response to stimulation and the bilateral R2. These responses represent a monosynaptic and polysynaptic circuitry for R1 and R2 respectively. The R1 response was considered to follow a trigeminal pathway in the pons while the R2 via a pathway adjacent the reticular formation reaches the facial nuclei.<ref>Ongerboer de Visser BW, Kuypers HG (1978): Late blink reflex changes in lateral medullary lesions. An electrophysiological and neuro-anatomical study of Wallenberg's syndrome. ''Brain'' '''101''': 285-294. </ref><ref>Ongerboer de Visser BW (1983b): Comparative study of corneal and blink reflex latencies in patients with segmental or with cerebral lesions. In: Desmedt JE , editor. ''Advances in neurology''. New York: Raven Press. p 757-772.</ref><ref>Ongerboer de Visser BW (1983b): Comparative study of corneal and blink reflex latencies in patients with segmental or with cerebral lesions. In: Desmedt JE , editor. ''Advances in neurology''. New York: Raven Press. p 757-772.</ref> | The blink is a reflex that is evoked by hitting the eyebrow region on one side of the forehead. Electrophysiologically it is possible to evoke it by applying an electrical stimulus on the eyebrow arch in correspondence with the supraorbital foramen. The responses are recorded through two surface electrodes positioned on the orbicularis oculi muscle on each side and the motor potentials can be mainly represented by two events, namely the ipsilateral R1 response to stimulation and the bilateral R2. These responses represent a monosynaptic and polysynaptic circuitry for R1 and R2 respectively. The R1 response was considered to follow a trigeminal pathway in the pons while the R2 via a pathway adjacent the reticular formation reaches the facial nuclei.<ref>Ongerboer de Visser BW, Kuypers HG (1978): Late blink reflex changes in lateral medullary lesions. An electrophysiological and neuro-anatomical study of Wallenberg's syndrome. ''Brain'' '''101''': 285-294. </ref><ref>Ongerboer de Visser BW (1983b): Comparative study of corneal and blink reflex latencies in patients with segmental or with cerebral lesions. In: Desmedt JE , editor. ''Advances in neurology''. New York: Raven Press. p 757-772.</ref><ref>Ongerboer de Visser BW (1983b): Comparative study of corneal and blink reflex latencies in patients with segmental or with cerebral lesions. In: Desmedt JE , editor. ''Advances in neurology''. New York: Raven Press. p 757-772.</ref> | ||
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