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ME12 Obstructive sleep apnea syndrome
S4
Abstracts of the 13th European Congress of Clinical Neurophysiology / Clinical Neurophysiology 119 (2008), S1–S131
ME11 Axonal excitability D. Burke Institute of Clinical Neurosciences, Royal Prince Alfred Hospital and University of Sydney, Australia Studies of the excitability of human axons using threshold tracking have now been established as reliable techniques that can provide insight into peripheral nerve dysfunction, complementing routine tests of nerve conduction [1]. The latter measure the ability of axons to conduct and their speed of conduction; the former provide information about the voltage-dependent conductances, pumps and other mechanisms responsible for maintaining membrane potential at the site of stimulation. The reliability of conclusions from these studies has been improved by the development of a computer model of the human large myelinated axon [2]. Threshold tracking relies on measuring the current required to produce a sub-maximal compound potential of designated amplitude (usually ∼40% of maximum because that is on the fast rising phase of the stimulus-response curve). Stimuli are delivered by a continuously variable constant-current source driven by specific software (Trond protocol of the Qtrac software © Professor Hugh Bostock, Institute of Neurology, London, UK). The testing protocol completes full studies of motor axon properties in normal subjects in ∼10 min. (i) The intensity of the test stimulus is varied (to produce a stimulus-response curve). (ii) Its width is varied (to define strength-duration properties). The test stimulus is conditioned by either (iii) subthreshold depolarizing and hyperpolarizing currents (to study threshold electrotonus and the current-threshold relationship), or (iv) a supramaximal conditioning stimulus (to document the recovery cycle). There have now been extensive studies in patients using these techniques [3]. References: [1] Kiernan MC et al. (2000) Muscle Nerve 23: 399-409. [2] Bostock H (2006) Clinical Neurophysiology;117: S85-86 [3] Lin CS-Y et al. (2006) In: Handbook of Clinical Neurophysiology, Vol. 7, Peripheral Nerve Diseases, Editor: Kimura J, pp. 381-403. Elsevier.
ME12 Obstructive sleep apnea syndrome E. Svanborg Dept. of Clinical Neurophysiology, University Hospital, Linköping, Sweden This lecture will give an overview of all aspects of current knowledge concerning the obstructive sleep apnea syndrome (OSAS). Definitions of apneas, hypopneas and other indices of respiratory distress will be given, as will the difference between pathology in recordings (obstructive sleep apnea, OSA) and the clinical entity OSAS. Different diagnostic methods such as oximetry, polygraphy and polysomnography will be described together with
scoring rules. Prevalence figures of the disorder in children, men and women in different age groups will also be mentioned. The aetiology of the disorder is not completely known, but in many cases there is a clear progression from habitual snoring without daytime fatigue to the typical OSAS. Snoring arises from vibration of the soft tissues in the upper airway. Patients working with vibrating tools often develop nervous lesions in the hands, and such lesions have been shown to be present in OSAS-patients and, to a lesser extent, habitual snorers. We therefore postulate that OSAS is caused by vibration-induced nervous lesions, which in turn causes upper airway collapse during sleep when muscle tone is naturally low. Neurophysiological methods to show such lesions in the upper airways will be described, n.b. EMG and measurement of cold perception thresholds. First-hand treatment of OSAS is currently CPAP, since adequate positive pressure appliance will abolish the apneas completely. The problem with this treatment is low patient compliance. Methods to improve this will be mentioned and also other treatment alternatives which may be pertinent, such as oral appliances if positional apnea is the main problem, or surgery if there are clear anatomical obstacles. Lastly, there is today robust evidence for a relationship between OSAS and cardiovascular morbidity and mortality, even in a dose-response fashion. It is therefore important that the neurophysiologist helps to make a correct and exact diagnosis.
ME13 Pathophysiology of dystonia A. Berardelli Department of Neurological Sciences, Sapienza, University of Rome, Italy Dystonia is a movement disorder characterized by twisting movements, especially during attempted movements, as well as abnormal postures, cocontraction activity and muscle spread to other regions of the body. Most of our knowledge of the pathophysiology of dystonia comes from neurophysiological investigations performed in patients with focal dystonias. In these latter conditions neurophysiological studies have demonstrated impaired inhibitory control of motor mechanisms at various levels of central nervous system, and abnormalities of somatosensory spatial and temporal discrimination. In the various clinical types of dystonia these abnormalities are present in affected and also in unaffected body parts and some of these abnormalities may be primary, rather than the consequence of dystonic activity. One possible meccanism for the pathophysiology of focal dystonia is an abnormal motor learning or an excessive neuroplasticity. Available data from recordings during surgery performed in patients affected by generalized dystonia have suggested a reduced GPi output to the thalamus, but additional changes in patterning and synchrony of neural discharges are also present.
Abstracts of the 13th European Congress of Clinical Neurophysiology / Clinical Neurophysiology 119 (2008), S1–S131
ME11 Axonal excitability D. Burke Institute of Clinical Neurosciences, Royal Prince Alfred Hospital and University of Sydney, Australia Studies of the excitability of human axons using threshold tracking have now been established as reliable techniques that can provide insight into peripheral nerve dysfunction, complementing routine tests of nerve conduction [1]. The latter measure the ability of axons to conduct and their speed of conduction; the former provide information about the voltage-dependent conductances, pumps and other mechanisms responsible for maintaining membrane potential at the site of stimulation. The reliability of conclusions from these studies has been improved by the development of a computer model of the human large myelinated axon [2]. Threshold tracking relies on measuring the current required to produce a sub-maximal compound potential of designated amplitude (usually ∼40% of maximum because that is on the fast rising phase of the stimulus-response curve). Stimuli are delivered by a continuously variable constant-current source driven by specific software (Trond protocol of the Qtrac software © Professor Hugh Bostock, Institute of Neurology, London, UK). The testing protocol completes full studies of motor axon properties in normal subjects in ∼10 min. (i) The intensity of the test stimulus is varied (to produce a stimulus-response curve). (ii) Its width is varied (to define strength-duration properties). The test stimulus is conditioned by either (iii) subthreshold depolarizing and hyperpolarizing currents (to study threshold electrotonus and the current-threshold relationship), or (iv) a supramaximal conditioning stimulus (to document the recovery cycle). There have now been extensive studies in patients using these techniques [3]. References: [1] Kiernan MC et al. (2000) Muscle Nerve 23: 399-409. [2] Bostock H (2006) Clinical Neurophysiology;117: S85-86 [3] Lin CS-Y et al. (2006) In: Handbook of Clinical Neurophysiology, Vol. 7, Peripheral Nerve Diseases, Editor: Kimura J, pp. 381-403. Elsevier.
ME12 Obstructive sleep apnea syndrome E. Svanborg Dept. of Clinical Neurophysiology, University Hospital, Linköping, Sweden This lecture will give an overview of all aspects of current knowledge concerning the obstructive sleep apnea syndrome (OSAS). Definitions of apneas, hypopneas and other indices of respiratory distress will be given, as will the difference between pathology in recordings (obstructive sleep apnea, OSA) and the clinical entity OSAS. Different diagnostic methods such as oximetry, polygraphy and polysomnography will be described together with
scoring rules. Prevalence figures of the disorder in children, men and women in different age groups will also be mentioned. The aetiology of the disorder is not completely known, but in many cases there is a clear progression from habitual snoring without daytime fatigue to the typical OSAS. Snoring arises from vibration of the soft tissues in the upper airway. Patients working with vibrating tools often develop nervous lesions in the hands, and such lesions have been shown to be present in OSAS-patients and, to a lesser extent, habitual snorers. We therefore postulate that OSAS is caused by vibration-induced nervous lesions, which in turn causes upper airway collapse during sleep when muscle tone is naturally low. Neurophysiological methods to show such lesions in the upper airways will be described, n.b. EMG and measurement of cold perception thresholds. First-hand treatment of OSAS is currently CPAP, since adequate positive pressure appliance will abolish the apneas completely. The problem with this treatment is low patient compliance. Methods to improve this will be mentioned and also other treatment alternatives which may be pertinent, such as oral appliances if positional apnea is the main problem, or surgery if there are clear anatomical obstacles. Lastly, there is today robust evidence for a relationship between OSAS and cardiovascular morbidity and mortality, even in a dose-response fashion. It is therefore important that the neurophysiologist helps to make a correct and exact diagnosis.
ME13 Pathophysiology of dystonia A. Berardelli Department of Neurological Sciences, Sapienza, University of Rome, Italy Dystonia is a movement disorder characterized by twisting movements, especially during attempted movements, as well as abnormal postures, cocontraction activity and muscle spread to other regions of the body. Most of our knowledge of the pathophysiology of dystonia comes from neurophysiological investigations performed in patients with focal dystonias. In these latter conditions neurophysiological studies have demonstrated impaired inhibitory control of motor mechanisms at various levels of central nervous system, and abnormalities of somatosensory spatial and temporal discrimination. In the various clinical types of dystonia these abnormalities are present in affected and also in unaffected body parts and some of these abnormalities may be primary, rather than the consequence of dystonic activity. One possible meccanism for the pathophysiology of focal dystonia is an abnormal motor learning or an excessive neuroplasticity. Available data from recordings during surgery performed in patients affected by generalized dystonia have suggested a reduced GPi output to the thalamus, but additional changes in patterning and synchrony of neural discharges are also present.