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Spindles and transients - Sleep Phenomena, Mechanisms and Substrates
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Spindles and transients - Sleep Phenomena, Mechanisms and Substrates

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This presentation discusses in detail the transients that occur mainly in late stage 1 and stage 2 of sleep, and may be confused to be pathological. The prototype here are theK complexes and the Sleep …

This presentation discusses in detail the transients that occur mainly in late stage 1 and stage 2 of sleep, and may be confused to be pathological. The prototype here are theK complexes and the Sleep Spindles.


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  • Incomplete synchrony, sparseness, also seen in vitro, higher synchrony seen during seizures
    Roaming cortical activation, perhaps semi-random to reactivate cortical circuits during slow wave sleep
    IMPORTANCE OF RT, inhibitory nucleus
  • A1g in dt, ai,h in nrt , leads to differences in bursts
    A1g yellow, a1h red, a1i blue
  • Inhibition, excitation, rebound burst firing resulting from t type ca channels, next
  • Transcript

    • 1. Electroencephalogram, Spindles and K complexes
    • 2. Sleep • The default state • Active Process • Requires synchronizers • Sleep Spindles, K Complexes
    • 3. Raphe promotes sleep Locus coeruleus promotes wakefulness *so sleep control is distributed across centers
    • 4. The reticular formation also promotes wakefulness
    • 5. Stages of sleep form cyclical pattern Slow-Wave Activity: -- Spindles: 7 - 15 Hz ; Wax and Wane -- Delta: 1 - 4 Hz -- Slow Osc. .5 - 1 Hz
    • 6. Sleep Spindles • Compared to alpha rhythm !! • One of the earliest described events • Hallmark of Synchronization • Requires an oscillator
    • 7. Midpontine pre- trigeminal Cerebellum Encephale isole‘ Klimesch VO: BioIII Normal sleep-wake cycle including REM Cerveau isole‘ SWS Thalamus Sleep-wake cycle without REM pproximate location of the three cuts for the human brain are below. 7
    • 8. THALAMUS
    • 9. Gyri orbitales Gyri frontales Co rp u G. praecentralis G. postcentralis RE Gyri temporales VA VL VP LP Pu LGN MGN Gyri parietales A M ss tri atu m
    • 10. Thalamocortical Network Ctx + + RE + TC -
    • 11. Thalamocortical spindle circuitry Modified from Steriade and Llinás. Physiol.Rev. 68:649-742, 1998.
    • 12. T type calcium channel genes in thalamus α1G α1H α1I Courtesy of E Talley, D Bayliss & E Perez-Reyes
    • 13. Post inhibitory rebound in thalamic relay neurons -60 Vm -70 -80 Ca2+depende nt rebound burst IPSP threshold 1 hT 0 T channels reprimed 100 ms
    • 14. Thalamo-cortical reentrant loops. Steriade, M. (1999). Coherent oscillations and short-term plasticity in corticothalamic networks. TINS, Vol. 22 (8), 337-344. Basic Circuitry: Cortex RE Cortex Dorsal Thal. = Relay Nuclei RE L-circ Th-cx Dendro-dendr. Th-cx RE L-circ Aff ‚Secondary neurons‘
    • 15. 1,2 Afferent brainstem input to Th-cx (1), Activation of RE and Cortex (2) Cortex L-circ RE Th-cx Dendro-dendr. Th-cx RE L-circ Aff
    • 16. 3 Excitatory processes in Cortex; Inhibition of primary L-circ; Inhibition of other RE cells Cortex L-circ RE Th-cx Dendro-dendr. Th-cx RE L-circ Aff
    • 17. 4 Excitatory feedback response from cortex. Disinhibition of primary L-circ neurons. Inhibition of secondary Th-cx neurons. The resulting effect is that during time 4, Th-cx are again under inhibitory control from L-circ neurons and, at the same time are activated from cortico-thalamic cells. Thus, only strong (converging and/or amplified) cortical feedback will trigger another excitatory activation wave into the cortex in time 5. Cortex The strong inhibition of the secondary Th-cx cell may lead to low threshold spikes (LTS) and, thus, to a 10 Hz oscillation. L-circ RE Th-cx Th-cx RE L-circ Aff
    • 18. 5 The primary Th-cx cell may start a new excitatory burst into the cortex. At this stage (because released from the L-circ inhibition), a new afferent input will have a strong effect. The secondary Th-cx cells remain under inhibition RESULT: Center-surround ‚on-off‘ effect with a resulting strong focal activation of cortical target neurons. Cortex RE L-circ Th-cx Th-cx RE L-circ Aff
    • 19. Summary of findings: Afferent brainstem activation is missing and cortical activation is strong: - Th-cx cells are hyperpolarized and oscillate with spindle frequency Note that a depol. current pulse during maximal hyperpol. leads to high frequency bursts. The result is increased oscillatory cortical activation leading to Delta activity. - The effect of increased cortical activation is even larger if stimulation patterns are oscillatory SLEEP: Spindles and Delta RE Cortex Th-cx hyperpolarized, Sleep spindles L-circ Th-cx Missing brainstem afferents
    • 20. Spindle oscillations in thalamus A M P A /N M D A R T h a la m u s G A B A AR nR t T C + timing R ebound B u rs t E P S P & B u rs t IP S P 20 m V C o rte x - 200 m s
    • 21. RE Cell Rapidly bursting type A Mathematical model Foundations II - Neuroimaging
    • 22. TC Cell modulation by RE cell A Mathematical model
    • 23. Propagation of Spindles
    • 24. Ontogeny of Spindles • EEG maturation • Posterior Dominant • Anterior spread • Amplitude decreases with age • Two ditinct frequency bands seen
    • 25. K Complexes Paroxysmal Events
    • 26. K Complexes • stage 2 sleep, arousing stimuli. • Loomis et al. (1938); • reason for calling them K complexes remains obscure • spur of the moment • Knocking • K complex shows a maximum over the vertex, • also K complexes with an indubitable maximum over the frontal midline.
    • 27. • H. Davis et al. - central and frontal K complexes • Brazier (1949) presumed two distinct generators; these were area 6, corresponding with the vertex, and area 9, corresponding with frontal midline. • initial sharp component, followed by a slow component that fuses with a superimposed fast component. • The sharp component is biphasic and not seldom multiphasic. • The slow component is represented by a large slow wave that may exceed 1,000 msec in duration
    • 28. Positive occipital sharp transients of sleep POSTS start to occur in healthy people at age 4 years, become fairly common by age 15 years, remain common through age 35 years, and start to disappear by age 50 years. POSTS are seen very commonly on EEG and have been said to be more common during daytime naps than during nocturnal sleep. Most characteristics of POSTS are contained in their name. They have a positive maximum at the occiput, are contoured sharply, and occur in early sleep (stages I and II). Their morphology classically is described as "reverse check mark," and their amplitude is 50-100 µV. They typically occur in runs of 4-5 Hz and are bisynchronous, although they may be asymmetric. They persist in stage II sleep but usually disappear in subsequent stag
    • 29. Vertex sharp transients Also called vertex waves or V waves, these transients are almost universal. Although they often are grouped together with K complexes, strictly speaking, vertex sharp transients are distinct from K complexes. Like K complexes, vertex waves are maximum at the vertex (central midline placement of electrodes [Cz]), so that, depending on the montage, they may be seen on both sides, usually symmetrically. Their amplitude is 50-150 µV. They can be contoured sharply and occur in repetitive runs, especially in children. They persist in stage II sleep but usually disappear in subsequent stages. Unlike K complexes, vertex waves are narrower and more focal and by themselves do not define stage II.