A peculiar rhythmic EEG activity from ventrobasal thalamus during paradoxical sleep in man

doi:10.1016/0013-4694(79)90213-X

Electroencephalography and Clinical Neurophysiology

Volume 47, Issue 2, August 1979, Pages 119-125

https://doi.org/10.1016/0013-4694(79)90213-X Get rights and content

Abstract

A peculiar 3/sec rhythmic EEG activity (named Vc rhythm) was consistently found at the ventrobasal thalamus (nucleus ventrocaudalis) during paradoxical sleep of patients with implanted electrodes used as an electrophysiological procedure for identification of the thalamic targets for the surgical treatment of tremor and rigidity.

The Vc rhythm was formed by high voltage, sharp biphasic positive negative potentials which were absent during wakefulness, rare and isolated during slow wave sleep, increased in number and organized in trains during paradoxical sleep and blocked during arousal. Significant changes in number of Vc waves were found when patients shifted through these wakefulness-sleep states. Integrated EMG multiple unit activity also showed significant changes during these wakefulness-sleep shifts, which were parallel although inverse to those showed by Vc waves.

A significant negative correlation (r = −0.7126) between number of Vc waves and EMG units was found. In contrast, Vc waves showed no correlation with other electrophysiological indicators of thalamic excitability (multiple unit activity and early evoked potentials) and sleep (scalp EEG frequency and ocular movements).

Résumé

Une activité EEG rythmique particulière à 3/sec (nommée rythme Vc) est constamment trouvée au niveau du thalamus ventrobasal (noyau ventro-caudal) au cours du sommeil paradoxal de malades porteurs d'électrodes implantées utilisées comme procédé électrophysiologique d'identification de la cible thalamique pour traitement chirurgical du tremblement et de la rigidité.

Le rythme Vc est constitué par des potentiels de haut voltage, aigus, biphasiques positifs-négatifs, qui ne s'observent pas au cours de l'état de veille, sont rares et isolés au cours du sommeil à ondes lentes, augmentent en nombre et s'organisent en bouffées au cours du sommeil paradoxal et sont bloqués lors de l'éveil. Des modifications significatives du nombre des ondes Vc s'observent au cours de ces stades veille-sommeil. L'activité multi-unitaire EMG intégrée montre également des modifications significatives au cours de ces variations veille-sommeil, qui sont parallèles, bien qu'inverses, à celles observées au niveau des ondes Vc.

Une corrélation négative significative (r = −0.7126) entre le nombre des ondes Vc et les unités EMG's observe. Par contraste, les ondes Vc ne montrent aucune corrélation avec d'autres indicateurs électrophysiologiques d'excitabilité thalamique (activité multi-unitaire et potentiels évoqués précoces) et du scalp (fréquence EEG et mouvements oculaires).

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Cited by (9)

Thalamic activity during scalp slow waves in humans
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Citation Excerpt :
A systematic study of invasive recordings from the human thalamus was reported already in the 1940s (Williams and Parsons-Smith 1949). Some further studies of sleep oscillations (Velasco et al., 2002; Velasco et al., 1979; Wennberg et al., 2002) and patterns of single-cell activity (Tsoukatos et al., 1997) in this structure were published decades ago. These findings confirmed that the thalamus – much like the cortex - exhibits different activity patterns across vigilance states, and that the morphology and temporal evolution of cortical and thalamic electroencephalographic signals are often similar.
Slow waves are major pacemakers of NREM sleep oscillations. While slow waves themselves are mainly generated by cortical neurons, it is not clear what role thalamic activity plays in the generation of some oscillations grouped by slow waves, and to what extent thalamic activity during slow waves is itself driven by corticothalamic inputs. To address this question, we simultaneously recorded both scalp EEG and local field potentials from six thalamic nuclei (bilateral anterior, mediodorsal and ventral anterior) in fifteen epileptic patients (age-range: 17–64 years, 7 females) undergoing Deep Brain Stimulation Protocol and assessed the temporal evolution of thalamic activity relative to scalp slow waves using time-frequency analysis. We found that thalamic activity in all six nuclei during scalp slow waves is highly similar to what is observed on the scalp itself. Slow wave downstates are characterized by delta, theta and alpha activity and followed by beta, high sigma and low sigma activity during subsequent upstates. Gamma activity in the thalamus is not significantly grouped by slow waves. Theta and alpha activity appeared first on the scalp, but sigma activity appeared first in the thalamus. These effects were largely independent from the scalp region in which SWs were detected and the precise identity of thalamic nuclei. Our results suggest that while small thalamocortical neuron assemblies may initiate cortical oscillations, especially in the sleep spindle range, the large-scale neuronal activity in the thalamus which is detected by field potentials is principally driven by global cortical activity, and thus it is highly similar to what is observed on the scalp.
The subcortical belly of sleep: New possibilities in neuromodulation of basal ganglia?
2020, Sleep Medicine Reviews
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Deep brain stimulation (DBS) is increasingly used to treat a variety of neurological disorders including Parkinson's disease, dystonia, tremor, pain, and epilepsy [18]. Several studies have utilised LFP recordings from externalised DBS electrodes with polysomnography to investigate the role of subcortical structures in sleep in humans [47,56,61–69]. In one of the earliest reports, Moiseeva et al. (1969) [61] described recordings during sleep from 11 patients, with electrodes in various locations including the subthalamic nucleus, pallidum, putamen, caudate nucleus, substantia nigra, ventrolateral and posterior thalamus and hypothalamus [61].
Early studies posited a relationship between sleep and the basal ganglia, but this relationship has received little attention recently. It is timely to revisit this relationship, given new insights into the functional anatomy of the basal ganglia and the physiology of sleep, which has been made possible by modern techniques such as chemogenetic and optogenetic mapping of neural circuits in rodents and intracranial recording, functional imaging, and a better understanding of human sleep disorders. We discuss the functional anatomy of the basal ganglia, and review evidence implicating their role in sleep. Whilst these studies are in their infancy, we suggest that the basal ganglia may play an integral role in the sleep-wake cycle, specifically by contributing to a thalamo-cortical-basal ganglia oscillatory network in slow-wave sleep which facilitates neural plasticity, and an active state during REM sleep which enables the enactment of cognitive and emotional networks. A better understanding of sleep mechanisms may pave the way for more effective neuromodulation strategies for sleep and basal ganglia disorders.
Temporo-spatial correlations between scalp and centromedian thalamic EEG activities of stage II slow wave sleep in patients with generalized seizures of the cryptogenic Lennox-Gastaut syndrome
2002, Clinical Neurophysiology
Citation Excerpt :
Fig. 1). All-night sleep studies were performed with the same technique used in our previous work on patients with depth electrodes (Velasco et al., 1979, 1980, 1989, 1995, 1997) following routine procedures (Rechtschaffen and Kales, 1995). Briefly, the studies were performed 17–24 days after electrode implantation and after 3 nights of laboratory habituation.
Objectives: Temporo-spatial correlations between scalp and centromedian thalamic (CM) normal and abnormal electroencephalographic (EEG) activities of stage II slow wave sleep (SWS II) were investigated in 5 patients with cryptogenic Lennox–Gastaut syndrome (CLGS).
Methods: In each patient, 8 h/all-night sleep studies were performed with routine methods; and a total of 1233 normal and 206 abnormal individual activities, spontaneously occurring during 200 epochs of early and late SWS II, were analyzed. Normal activities included scalp-CM K-complexes (KC-CMKC), vertex waves (VW-CMVW), and sleep spindles (SS-CMSS). Abnormal activities included: thalamo-cortical spikes (TCS-CMTCS), and epileptic (EPKC-CMEPKC) and W K-complexes (WKC-CMWKC).
Results: (1) All abnormal and normal spontaneous SWS II activities occurred associated in scalp and CM regions except the SS. Associated spindles were significantly larger (P<0.01) than dissociated ones, this occurring during both early and late SWS II. (2) The peak of VW significantly anticipated (P<0.02) that of its CM counterpart (CM-VW), while the peak of CMTCS anticipated that of its scalp counterpart. The onset of CMSS significantly anticipated (P=0.02) that of its scalp counterpart (SS). The behavior of VW-CMVW and TCS-CMTCS of the abnormal KC was similar to those of the normal complexes, while the onset of abnormal spindles was simultaneous in scalp and CM regions. Scalp VW, CTS, and SS attained maximal amplitude at the parietal region bilaterally with decreasing amplitude gradients to other scalp regions, while CMVW, CMTCS, and CMSS attained maximal amplitude in all thalamo-mesencephalic regions of CM. (3) Normal spindles significantly reduced (P<0.02) the amplitude of the positive CM, CMVW, and scalp TCS counterparts of the negative scalp VW and CM (CMTCS), respectively, while abnormal spindles reduced the amplitudes (P<0.01) of both negative VW and CMTCS and positive counterparts.
Conclusion: These data suggest the following: (1) that all SWS II activities, including SS, are mediated by common thalamo-cortical systems; (2) that VW originate from the parietal scalp and normal spindles and TCS from the CM regions bilaterally while abnormal spindles originate either from widespread cortical and CM regions or from a site outside the thalamo-cortical systems, and (3) that the functional role of SS is to inhibit non-specific thalamo-cortical systems for sleep preservation.
Rapid-eye-movement sleep involves the memory-conversion circuits in a brain model
2000, Medical Hypotheses
People can remember the content of a dream in rapid eye movement (REM) sleep but cannot do so in slow-wave sleep. According to a brain model, memory is stored in encoding synapses as presynaptic axonal ‘on–off’ patterns and modulating synapses help encoding synapses convert short-term memory into long-term memory. These lead to the hypothesis that REM sleep involves modulating synapses of the memory-conversion circuits including the anterior nuclei and dorsomedial nuclei of the thalamus. Cortical neurons get more rest in slow-wave sleep than in REM sleep. The locus coeruleus, raphe nuclei, and tuberomammillary nuclei get more rest during REM sleep when these nuclei cease to fire. The paralyses of peripheral muscles during REM sleep and cataplexy, and cessation of chorea, athetosis, hemiballismus, and parkinsonism tremor during sleep may result from spinal cord inhibition by the gigantocellular nuclei and raphe nuclei at the reticular formation. Sleep and wake relate to the light–dark cycle on the Earth. Were the light–dark cycle 50 hours a day, the human circadian clock might be around 50 hours. With increasing use of artificial light to keep people awake at night, it may affect the circadian rhythm and firing rate of neurons, the presynaptic axonal ‘on–off’ patterns as content of consciousness, and the mood.
Effect of a new thienodiazepine (We-941) on sleep patterns of normal and insomniac subjects
1981, Neuropharmacology
The effect of a new thienodiazepine We-941 (0.5 mg, oral) on sleep patterns of normal and insomniac subjects was quantitatively determined and statistically compared with (a) the sleep patterns obtained under base line conditions and with placebo in 10 normal subjects; (b) with those obtained under initial and final placebo in a series of 8 insomniac subjects; and (c) with those obtained with flurazepam (30 mg, oral) in another series of 8 insomniac subjects.
- 1.
  1. The spontaneous arousal episodes shown by some normal subjects under base line conditions and with placebo were abolished by We-941. However, no significant differences in wakefulness-sleep parameters were found in normal subjects under We-941 compared with base line or placebo.
- 2.
  2. The duration of wakefulness and number of arousal episodes were decreased by We-941 which increased the duration of sleep, decreased the latency of slow wave sleep I and II and increased the duration of slow wave sleep III. These results were significantly different to initial, but not to final, placebos in the same insomniac subjects.
  Flurazepam decreased the duration of wakefulness and number of arousal episodes and increased the duration of sleep and duration of rapid eye movement sleep. These results were significantly different from initial, but not from final, placebos in the same insomniac subjects.
- 3.
  3. No significant differences were found between the effects of We-941 and flurazepam on slow wave sleep III and rapid eye movement sleep in different insomniac subjects.
Wakefulness-sleep modulation of cortical and subcortical somatic evoked potentials in man
1980, Electroencephalography and Clinical Neurophysiology
Amplitude changes of early and late components of cortical and subcortical somatic evoked potentials (SEP) were determined during wakefulness-sleep steady state shifts in patients with implanted electrodes used as an electrophysiological procedure for the surgical treatment of unilateral tremor and rigidity. SEP were produced by threshold motor stimulation of the median nerve and simultaneously recorded from contralateral scalp, thalamic and subthalamic regions, while patients spontaneously shifted from initial wakefulness (W1), to slow wave sleep (SWS I, II, IV), paradoxical sleep (PS) and final wakefulness (W2).
- 1.
  (1) During W1, cortical responses were formed by early (P50) and late (P100, 200, 300) components. Subcortical type A responses were formed only by early (N or P20) components recorded within a circumscribed region including VPL thalamic nucleus and medial lemniscus. Subcortical type B and C responses were formed by only late components (P100 and P100, 300 respectively) and were recorded intermixed within a widespread region including VL and Ce thalamic nuclei, zona incerta, nucleus subthalamicus, prelemniscal radiations and reticular formation.
- 2.
  (2) Early cortical and subcortical components significantly increased when patients shifted from PS to W2 but showed no systematic changes during other wakefulness-sleep state shifts.
- 3.
  (3) Late cortical and subcortical components significantly decreased when patients shifted from W1 to SWS I and increased from PS to W2. In addition, late cortical components significantly decreased from SWS I to II and remained unchanged from SWS II to IV while late subcortical components remained unchanged from SWS I to II and significantly decreased from SWS II to IV. These components were maximally depressed during SWS IV and PS; however new cortical (P150, N250, P450) and subcortical (P250 or N300) components appeared during SWS IV but not during PS.
Les modifications d'amplitude des composantes précoces et tardives des potentiels évoqués somatiques corticaux et sous corticaux (SEP) sont mesurées au cours des changements entre états stables veille-sommeil chez des patients avec électrodes implantées, utilisées comme procédure électrophysiologique pour traitement chirurgical de tremblement et de rigidité unilatéraux. Les SEP sont provoqués par stimulation au seuil moteur du nerf médian et sont enregistrés simultanément sur le scalp controlatéral, au niveau des régions thalamiques et sous-thalamiques alors que les patients varient spontanément de la veille initiale (W1) au sommeil à ondes lentes (SWS I, II, IV), au sommeil paradoxal (PS) et à la veille finale (W2).
- 1.
  (1) Au cours de W1, les réponses corticales sont constituées par des composantes précoces (50) et tardives (P100, 200, 300). Les réponses sous-corticales de type A ne sont constituées que par des composantes précoces (N ou P20) enregistrées à l'intérieur d'une région limitée qui inclut les noyaux thalamiques VPL et lemniscus médian. Les réponses sous-corticales de type B et C ne sont constituées que par des composantes tardives (P100 et P100, 300 respectivement) et sont enregistrées de façon mélangée à l'interiéur d'une large région qui inclut les noyaux thalamiques VL et Ce, la zona incerta, le noyau sous-thalamique, les radiations prélemniscales et la formation réticulaire.
- 2.
  (2) Les composantes corticales et souscorticales précoces augmentent de façon significative lorsque les malades passent de PS à W2 mais ne montrent aucune modification systématique au cours des variations d'autres états veille-sommeil.
- 3.
  (3) Les composants corticales et souscorticales tardives diminuent de façon significative lorsque les patients passent de W1 à SWS I et augmentent lors du passage de PS à W2. De plus, les composantes corticales tardives diminuent de façon significative au passage de SWS I à II et restent inchangées au passage de SWS II à IV tandis que les composantes sous-corticales tardives restent inchangées au passage de SWS I et II et diminuent de façon significative au passage de SWS II à IV. Ces composantes sont déprimées au maximum au cours de SWS IV et PS, bien que de nouvelles composantes corticales (P150, N250, P450) et sous-corticales (P250 ou N300) apparaissent au cours de SWS IV mais pas au cours de PS.

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A peculiar rhythmic EEG activity from ventrobasal thalamus during paradoxical sleep in manActivité EEG rythmique particulière provenant du thalamus ventrobasal au cours du sommeil paradoxal chez l'homme

Abstract

Résumé

Electroenceph. clin. Neurophysiol.

Electroenceph. clin. Neurophysiol.

Electroenceph. clin. Neurophysiol.

Electrophysiological technique used to differentiate thalamic nuclei

Physiologie und Pathophysiologie der tiefen Strukturen des menschlichen Gehirns

Anatomy of the thalamus

Thalamic units involved in somatic sensation and voluntary and involuntary movements in man

Neurophysiology of the states of sleep

Physiol. Rev.