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INTRODUCTION: The noninvasive evaluation of the autonomic nervous system (ANS) has been developed in the last decades. The implementation of an specialized unit requires qualified personnel, adequate equipment, location and support. The purpose of the present review is to summarize some theorical and practical aspects of 11 years experience in an ANS Section within a Neurophysiology Department. DEVELOPMENT: During this time we have examined 4,082 patients, using the basic reflex screen in 58% of them with a mean of 100 minutes and 159 Euros per patient. When other types of tests were applied, the time consumed oscillated between 75 and 300 minutes. The patients age ranged from 1 to 91 years, 8% of children among them. From 4,082 patients, the screen was conclusive with some condition related to ANS in 34% of them. The most frequent cause of ANS evaluation was the existence of dizziness, loss of consciousness of unknown origin or syncopal episodes (72%). When patients had at least one spell, sincopal or not, the evaluation was positive in 43%. Patients came from Neurology (67%), Cardiology (8%), Otorhinolaryngology (8%), Endocrinology (7%), and other Departments (10%). CONCLUSION: The different disciplines dealing with autonomic functions promote the diverse origin of autonomic evaluation demand. We suggest the convenience of making an accurate estimation of tests, time and cost per patient, to achieve the best unit management.

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Introducción. Las técnicas de estudio del sistema nervioso autónomo (SNA) por métodos no invasivos se han desarrollado a lo largo de las últimas décadas. La puesta en marcha de una unidad específica requiere recursos humanos cualificados, infraestructura y equipamiento. El objetivo del presente trabajo es revisar aspectos teóricos y prácticos sobre la experiencia de 11 años de funcionamiento de una sección dedicada al estudio del SNA, implantada en un Servicio de Neurofisiología Clínica. Desarrollo. Se han atendido 4.082 pacientes a los que, con mayor frecuencia, se aplicó el estudio básico SNA (58 por ciento), en el que se invierte una media de 100 minutos, con un coste por proceso de 159 EUR. Cuando se utilizaron otras pruebas, el tiempo osciló entre 75 y 300 minutos. La edad de los pacientes es de 1-91 años, con un 8 por ciento de pacientes pediátricos. El estudio SNA resultó patológico en el 34 por ciento de los casos. El motivo de consulta más frecuente fue el relacionado con mareos y pérdida de conciencia de origen indeterminado o con clínica sincopal (72 por ciento). De los pacientes que habían sufrido al menos una pérdida de conciencia, sincopal o no, el estudio SNA resultó positivo en el 43 por ciento de los casos. Los pacientes se remitieron desde Neurología (67 por ciento), Cardiología (8 por ciento), Otorrinolaringología (8 por ciento), Endocrinología (7 por ciento) y otros (10 por ciento). Conclusiones. Las diferentes disciplinas involucradas con las funciones autonómicas son la causa de la diversidad de procedencia de las peticiones de estudio. Señalamos la conveniencia de llevar a cabo una imputación individualizada de pruebas, tiempo y coste por paciente (AU)

Introduction. The noninvasive evaluation of the autonomic nervous system (ANS) has been developed in the last decades. The implementation of an specialized unit requires qualified personnel, adequate equipment, location and support. The purpose of the present review is to summarize some theorical and practical aspects of 11 years experience in an ANS Section within a Neurophysiology Department. Development. During this time we have examined 4,082 patients, using the basic reflex screen in 58% of them with a mean of 100 minutes and 159 Euros per patient. When other types of tests were applied, the time consumed oscillated between 75 and 300 minutes. The patients age ranged from 1 to 91 years, 8% of children among them. From 4,082 patients, the screen was conclusive with some condition related to ANS in 34% of them. The most frequent cause of ANS evaluation was the existence of dizziness, loss of consciousness of unknown origin or syncopal episodes (72%). When patients had at least one spell, sincopal or not, the evaluation was positive in 43%. Patients came from Neurology (67%), Cardiology (8%), Otorhinolaryngology (8%), Endocrinology (7%), and other Departments (10%). Conclusion. The different disciplines dealing with autonomic functions promote the diverse origin of autonomic evaluation demand. We suggest the convenience of making an accurate estimation of tests, time and cost per patient, to achieve the best unit management (AU)

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BACKGROUND AND AIM: Thalamic and brainstem strokes are a cause of organic hypersomnia. In thalamic lesions it has been attributed to disruption of ascending activating impulses from the brainstem reticular formation and to insufficient spindling and slow-wave production, which depends upon activities of reticular thalamic nucleus and thalamocortical neurons, respectively. Reported sleep disorders in brainstem lesions have occasionally been contradictory and that is because of the presence of nearby structures in the brainstem with different functions in sleep-waking cycle. The aim of the study is to present the results of polysomnographic records in patients with thalamic and/or brainstem vascular lesions, and to correlate them with the anatomical structures affected. PATIENTS AND METHODS: We have performed a polysomnographic study, (8-channel system), in patients with thalamic and/or brainstem strokes. All of them showed alterations of sleep-wake cycle. Neuroimaging studies were carried out in all patients. RESULTS: We report seven patients, 4 males and 3 females. Two cases presented thalamic strokes, in 3 the lesion was located in the brainstem and 2 patients had thalamo-mesencephalic lesions. All of them developed hypersomnia with an increase of NREM sleep. In patients with bilateral mesencephalic lesions we found that REM sleep was diminished as well. CONCLUSIONS: We have confirmed that lesions affecting thalamus and mesencephalic or pontine tegmental reticular formation are a cause of hypersomnia. The observation that this sleepiness is transient, supports the evidence of an extrathalamic alternative activating route.

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This study examines the influence of lesions in the centralis superior raphe nucleus (CeSR) and adjacent paramedial pontine tegmentum on the sleep/wakefulness cycle (SWC) in cats. Sixteen cats had electrodes implanted for electro-oculogram (EOG), electromyogram (EMG), electroencephalogram (EEG) and ponto-geniculo-occipital (PGO) recordings. There were 10 experimental animals: seven animals received diathermocoagulation lesions destroying between 7 and 27% of the CeSR; the remaining three cats suffered bilateral lesions in the paramedial portion of the reticularis pontis oralis (RPO) and caudalis (RPC) nuclei. Six sham-operated animals were used as controls. Recordings were taken of all animals in continuous 23-h sessions once a week for 12 weeks. Results indicated that the threshold for SWC state changes (increase of wakefulness (W) and drowsiness (D), and decrease of slow wave sleep (SWS)) after CeSR lesion is approximately 11.3% following volumetric destruction of the nucleus. The amount of CeSR damage (CeSR-D) only correlated significantly with the amount of W (positive correlation) and SWS (negative correlation) during the first week post-lesion. The changes in W over the course of the study were different in the two experimental groups. In both groups, total W was increased with respect to the controls, however, these increases were observed earlier in the CeSR-D group. The return to near control values in SWC state over days 15-28 of the study does not represent a definitive recovery by the CeSR-D cats. All the SWC states returned to control values by the tenth week in the cats with paramedial reticular pontine damage.

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Forty subjects were clinically examined using scales for cerebellar, pyramidal, parkinsonian, and mental status and by quantitative evaluation of neuroimages. The patients were classified into two groups: cerebellar-plus and "pure" cerebellar syndromes. Patients with "pure" cerebellar syndrome were diagnosed as autosomal dominant cerebellar ataxia III (ADCA III) or "pure idiopathic" late-onset cerebellar ataxia (ILOCA) in this series. Patients with cerebellar-plus syndrome were diagnosed as multiple system atrophy (MSA), subclassified as either ILOCA-plus, ADCA I, ADCA II or autosomal recessive LOCA. We have used visual (VEP), brainstem auditory (BAEP) and somatosensory (SEP) evoked potentials in order to establish their diagnostic validity. Cerebellar-plus syndrome and "pure" cerebellar syndrome showed overlapping VEP, BAEP and SEP abnormalities. VEP P100 latency, however, shows a certain ability to differentiate between the two groups (p = 0.08) and appears useful in distinguishing between sporadic cerebellar-plus syndromes (MSA or ILOCA-plus) and "pure" cerebellar syndromes (p < 0.02). The incidence of prolonged N9-N13 latency was significantly higher in the latter subgroup (p < 0.04) as well. Within cerebellar-plus syndromes, VEP, BAEP and SEP abnormalities were more frequent in inherited cases (ADCA I and II, along with autosomal recessive LOCA) than in sporadic ones. The most apparent differences were a higher incidence of abnormal BAEPs at brainstem level (p < 0.002), and of both peripheral and possible central SEP impairment in hereditary cerebellar-plus syndrome than in sporadic cerebellar-plus syndrome (p < 0.03). EP investigation is useful to a certain extent in differentiating between some variants of LOCA.

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We describe polysomnographic studies of a 44 years-old man who showed a defect in the central nervous regulation of the sleep-waking cycle (SWC), hypoventilation and cardiovascular hyperactivity after a right-sided tegmental pontine hematoma. A significant increase in total sleep time mainly depending upon stage 1 + 2 was observed. Predominant unilateral damage to the medial and central region of the reticularis pontis oralis (Poo) nucleus, extending into the central part of the rostral reticularis pontis caudalis (Poc) nucleus, was presumably responsible for the hypersomnia in this patient.

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Acute confusional state following metrizamide myelography has been reported to occur in up to 2% of patients. These patients have been diagnosed as having toxic encephalopathy. Recently, various cases have been reported to have a nonconvulsive status (absence status or complex partial status) who responded well to diazepam or clonazepam therapy. However, some authors have described cases of nonresponders to anticonvulsive therapy. Failure of therapy can be dose-related. For this reason, our patient was closely monitored by EEG to determine if dose adjustment was warranted, thereby achieving good results.

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