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[0] Bevan MD, Magill PJ, Terman D, Bolam JP, Wilson CJ, Move to the rhythm: oscillations in the subthalamic nucleus-external globus pallidus network.Trends Neurosci 25:10, 525-31 (2002 Oct)[1] Bevan MD, Magill PJ, Hallworth NE, Bolam JP, Wilson CJ, Regulation of the timing and pattern of action potential generation in rat subthalamic neurons in vitro by GABA-A IPSPs.J Neurophysiol 87:3, 1348-62 (2002 Mar)[2] Magill PJ, Bolam JP, Bevan MD, Dopamine regulates the impact of the cerebral cortex on the subthalamic nucleus-globus pallidus network.Neuroscience 106:2, 313-30 (2001)[3] Magill PJ, Bolam JP, Bevan MD, Relationship of activity in the subthalamic nucleus-globus pallidus network to cortical electroencephalogram.J Neurosci 20:2, 820-33 (2000 Jan 15)

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ref: -0 tags: buszaki watson oscillations review gamma theta hippocampus cortex date: 09-30-2013 18:32 gmt revision:2 [1] [0] [head]

PMID-23393413 Brain rhythms and neural syntax: implications for efficient coding of cognitive content and neuropsychiatric disease.

  • His frequency band standards:
    • delta: 1.5 - 4Hz
    • theta: 4 - 10Hz
    • beta: 10 - 30 Hz
    • gamma: 30 - 80Hz
    • fast: 80 - 200 Hz
    • ultra fast: 200 - 600 Hz.
  • comodugram: power-power correlelogram
  • Reviews current understanding of important rhythms:
    • How gamma is preserved amongs mammals, owing to the same fundamental mechanisms (membrane time constant, GABA transmission, AMPA receptior latency) all around 25ms; suggests that this is a means of tieing neurons into meaningful groups. or symbols; (solves the binding problem?)
    • Theta rhythm, in comparison, varies between species, inversely based on the size of the hippocampus. Larger hippocampus -> greater axonal delay.
    • These and other the critical step is to break neurons into symbols (as part of a 'language' or sequenced computation), not arbitrarily long trains of spikes which are arbitrarily difficult to parse.
  • Reviews the potential role of oscillations in active sensing, though with a rather conjectorial voice: suggests that sensory systems
  • Suggests that neocortical slow-wave oscillations during sleep are critical for transferring information from the hippocampus to the cortex: the cortex become excitable at particular phases of SWS, which biases the fast ripples from the hippocampus. During wakefulness, the direction is reversed -- the hippocampus 'requests' information from the neocortex by gating gamma with theta rhythms.
  • "Typically, when oscillators of different freqencies are coupled, the network oscillation frequency is determined by the fastest one. (??)
  • I actually find figure 3 to be rather weak -- the couplings are not that obvious, espeically if this is the cherry-picked example.
  • Cross phasing-coupling, or n:m coupling: one observes m events associated with the “driven” cycle of one frequency occurring at n different times or phases in the “stimulus” cycle of the other.
    • The mechanism of cross-frequency coupling may for the backbone of neural syntax, which allows for both segmentation and linking of cell assemblies into assemblies (leters) and sequences (words). Hmm. this seems like a stretch, but I am ever cautious.
  • Brain oscillations for quantifiable phenotypes! e.g. you can mono-zygotic twins apart from di-zygotic twins.

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ref: Rosin-2011.1 tags: PD closed loop DBS globus pallidus oscillations STN Vaadia heterodyne beta date: 03-26-2012 16:23 gmt revision:16 [15] [14] [13] [12] [11] [10] [head]

PMID-22017994[0] Closed-loop deep brain stimulation is superior in ameliorating parkinsonism.

  • Also reviewed by Rui Costa: PMID-22017983[1]
    • Good, brief review -- with appropriate minimal references.
  • Partial goal of the work: parameter determination and optimization can take a long time, and are typically only done every 3-6 months initially. But the actually changes of activity / responsiveness occur on a faster timescale in the disease, even instantaneous; other studies have shown that updating the stimulation parameters more frequently helps patients. (of course, this is a different form of closed-loop).
  • Pathology: intermittent neuronal oscillations in the basal ganglia and motor cortex commonly observed.
    • In MPTP treated primates these oscillations occur in the tremor band (theta, 4-7Hz), and double-tremor band (9-15Hz, alpha) (Bergman et al 1994 {120}, Ras et al 2000 PMID-11069964 ).
    • Actual pathology still inconclusive; talk about disruption of pathological patterns and 'focal inhibition', but this is no thorough review by any estimate.
  • "In recent years, the role of pathological discharge patterns in the parkinsonian brain has emerged as pivotal in the disease pathology
    • Eusebio and Brown, 2007;
    • Hammond et al., 2007;
    • Kuhn et al., 2009;
    • Tass et al., 2010;
    • Vitek, 2008;
    • Weinberger et al., 2009;
    • Wichmann and DeLong, 2006;
    • Zaidel et al., 2009.
    • Automatic systems should disrupt this pattern of discharge (Feng 2006, Tass 2003).
      • However, the role of these oscillations as the neuronal correlate of PD motor symptoms is still debated (Hammond et al., 2007; Leblois et al., 2007; Lozano and Eltahawy, 2004; McIntyre et al., 2004; Tass et al., 2010; Vitek, 2002; Weinberger et al., 2009 {1089}).
  • 2 african green monkeys, MPTP treatment.
  • Recorded from GPi & M1 (127 and 210 neurons); stimulated GPi, 7 pulses at 130Hz, 80ms after spike from reference area (M1 or GPi).
    • 80ms delay coincided with the next double-tremor oscillatory burst (12.5Hz)
    • State of neuronal oscillatory discharge of cortico-BG loops often accompanied by synchronization btw cortex and BG (see also quote below)
    • GPi following M1 activity superior (GP|M1 in their notation).
    • single pulses did not work.
    • Stimulation: 80uA 200us bipolar biphasic (small and short!).
  • Stimiulus protocol (M1 trigger) abolishes oscillatory activity in recorded GPi neurons.
  • Also reduced akinesia as measured with an accelerometer & decreased firing rate in the GPi.
    • Both work better than constant 130Hz DBS.
    • Also much more irregular: fewer stimulation pulses at longer latency.
  • Open loop control (the control) did much less regarding FR oscillations & bursts and reduction in firing rate.
    • Dorval et al 2010: increasing the stimulus irregularity of open-loop DBS decreases its beneficial clinical effectcs. (also Baker et. al 2011).
  • GP train stimulation triggered on GP firing significantly worsened akinesia, despite the fact that the pallidial FR decreased.
    • Treatment increased spike oscillation at double-tremor frequency in M1.
  • Oscillations more important than firing rate changes (new vs. old hypothesis).
    • pallidal oscillatory activity was not correlated to the pallidal discharge rate either before or during the application of standard DBS or GP|M1.
  • In our data, may have double-frequency tremor effects. Heterodyne should detect this.
    • "Studies on the dynamics of the entire cortico-basal ganglia loops have frequently reported the emergence of intra-and interloop component synchrony and oscillatory activity."
    • "Nevertheless, the somewhat intuitive connection between neuronal oscillations and parkinsonian motor symptoms, which include rest and action tremors, has been challenged (Hammond et al., 2007 PMID-17532060 ; Leblois et al., 2007 {1146}; Lozano and Eltahawy, 2004; Tass et al., 2010 {1147}; Vitek, 2002; Weinberger et al., 2009). For instance, while the parkinsonian rest tremor occurs mainly at the 4–7 Hz frequency band, the oscillatory neuronal activity is observed in several characteristic frequency bands in both human PD patients (Hutchison et al., 2004) {1156} and animal models (Bergman et al 1994, Gubellini et al 2009) {1074}"
      • This also has import to our heterodyne results!
    • Synchrony between globus pallidus and M1 is dynamic and state-dependent (whatever that means -- have to check the refs, Levy et al 2002 {829}, Timmerman et al 2003 {1087})
  • Quote: "... it suggests that reduction of the abnormal parkinsonian oscillatory activity could in fact be the underlying mechanism by which DBS exerts its action and brings about the associated clinical improvement."
  • Neuronal oscillatory activity occurs as high as the beta-band, 15-35Hz, hence clinical app. would need a tuned antiphase lag.
  • Suggest that the closed-loop treatment may be applicable to other diseases with characteristic firing patterns, like schizophrenia.
  • Since synchonization and oscillations hend to coincide, .. we found this too.
    • Heimer et al 2006 {1076}: oscillations and synchrony can exist independently.
  • Figure suck. Text inconsistent and frequently too small.
    • Wavelet spectrograms are nice tho.

Other thoughts:

  • Somebody should measure the transfer function of the BG / cortical loop. H(z).
  • This seems like adding a comb-filter or zero at a particular frequency: GP|GP stimluation exacerbated the effect, GP|M1 minimized the effect as there is a negation in there. (e.g. GP actviity decreases firing of M1, and vice versa).


[0] Rosin B, Slovik M, Mitelman R, Rivlin-Etzion M, Haber SN, Israel Z, Vaadia E, Bergman H, Closed-loop deep brain stimulation is superior in ameliorating parkinsonism.Neuron 72:2, 370-84 (2011 Oct 20)
[1] Santos FJ, Costa RM, Tecuapetla F, Stimulation on demand: closing the loop on deep brain stimulation.Neuron 72:2, 197-8 (2011 Oct 20)

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ref: -0 tags: Hutchison oscillations basal ganglia beta gamma globus pallidus date: 03-26-2012 16:21 gmt revision:2 [1] [0] [head]

PMID-15496658 Neuronal oscillations in the basal ganglia and movement disorders: evidence from whole animal and human recordings.

  • This is a review / mini-symposium (only 3 pages)
    • Cites other Hutchison papers: 1997, 1998.
  • Critique classical hypothesis in that GPi firing does not increase that much, 10-22% in animal models. IT explains akinesia and bradykinesia, but not rigidity or tremor. (This was 8 years ago, remember!)
    • Plus, most neurons have intrinsic pacemaker-like properties that sets the rate of firing in the absence of synaptic input. (Bevan et al 2002).
  • Oscillations:
    • Alpha band enhanced after MPTP treatment in green monkeys and in the STN of some PD patients with tremor at rest.
    • Higher frequency oscillations (beta, 15-25Hz) can be observed in some patients without resting tremor.
    • Much slower oscillations discovered by Judith Walters, 6 OHDA rat (0.3 - 2Hz).
    • Also ultralow, multisecond oscillations, which appear in dopamine stimulated rats. (Ruskin et al 1999a,,b, 2003).
      • Lesion of the STN was not found to change these ultralow oscillations, but did modify the connectivity between GP and SNr.
    • Courtemanche et al 2003 studied the possible normal physiological function for oscillations in basal ganglia networks.
      • Beta band decreased during saccadic eye movements.
      • LFP syncronization showed task-related decrease, but only in sites engaged in the task, as evicenced by saccade-related activity.
  • Boraud tested gradual small-dose administration of MPTP toxin:
    • Minimal changes in the average firing rate of GPi neurons
    • Oscillatory activity between 4-9 and 11-14 Hz, with differences between monkeys.
      • Oscillations increased with symptom presentation.
  • Goldberg et al 2004: analyzed coherence between EEG and BG LFP; surmise that in the PD condition the basal ganglia and cortex become more closely entrained by global brain dynamics, which are reflected in the widespread local field potentials.
  • Peter Brown: oscillations in the beta band are enhanced to such an extent in Parkinson's disease that voluntary movements are not generated because motor command for initiation cannot override the enhanced oscillatory state.
    • That is, movement initiation corresponds to beta-band desynchronization, and movement command cannot 'break through'.

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ref: -0 tags: hippocampus theta oscillations memory date: 03-18-2012 18:09 gmt revision:0 [head]

PMID-21696996 The hippocampus: hub of brain network communication for memory

  • Their hypothesis: memory encoding is dominated by theta oscillations 6-10 Hz; during inactivity, hippocampal neurons burst synchronously, creating sharp waves, theoretically supporting memory consolidation.
  • (They claim): to date there is no generally accepted theoretical view on memory consolidation.
  • Generally it seems to shift from hippocampus to neocortex, but still, evidence is equivocal. (Other than HM & other human evidence?)
  • Posit a theory based on excitation ramps of reverse-replay, which seems a bit fishy to me (figure 3).
  • Didn't know this: replay in visual and PFC can be so precise that it preserves detailed features of the crosscorrelograms between neurons. [58, 65, 81].

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ref: -0 tags: hippocampus theta oscillations date: 03-18-2012 17:34 gmt revision:2 [1] [0] [head]

PMID-11832222 Theta Oscillations in the Hippocampus

  • Theta-alpha oscillations have been found in 'all mammals to-date, including humans. (Hence conserved, hence possibly essential).
    • Prevalent in REM sleep.
    • Present in slices bathed in carbachol, too.
    • As well as locomotor activities; but not usually when the animal is resting.
  • Other reviews: Bland 1986, VAnderwolf 1988, Lopes da Silva et al 1990, Buzaki et al 1994 Stewart and Fox 1990, Vinogradova 1995, Vertex and Kocsis 1997.
    • Modeling reviews used passive cable properties; actually, it seems neurons, and their dendrites are have active conductances & active oscillatory features.
  • Theta oscillations most strongly present in CA1
  • Along similar lamina, oscillations are similar.
  • Osc. visible in cortical structures ...
    • subicular complex, entorhinal cortex, perirhinal cortex, cingulate cortex, amygdala -- though none of these structures are capable of generating theta oscillations intrinsically.
  • Also apparent in subcortical structures,
    • Dorsal raphe nucleus, ventral tegmental nucleus, and anterior thalamic nuclei. None of these seem required for oscillation, however:
  • Oscillations may emanate from the medial-septum-diagonal band of Broca (MS-DBB); lesion inactivates theta oscillations in all cortical areas, but the relative role is uncertain, as MS-DBB oscillations may require hippocampal and entorhinal afferents.
    • EPSPs brought about by the MS-DBB cholinergic neurons on hippocampal pyramidal cells cannot be responsible for the atrophine-sensitive form of theta.
    • That said, even though atrophine treatment only modestrly affects theta, it is reduced several-fold after selective neurotoxin elminiation of MS-DBB cholinergic cells -- maybe it's nicotinic synapses?
  • Drugs:
    • Theta can be blocked by GABA antagonist (picrotoxin, induces epilepsy) or agonist (pentoparbital anesthesia).
    • Many other drugs affect oscillations.
    • Broken down into atrophine-sensitive and atrophine-resistant oscillations.
      • (Atrophine blocks muscarinic Ach receptors).
    • Amplitude and frequency of theta does not appreciably change even after large doses of systematic muscarinic blockers.
      • Same drugs abolish theta under anesthesia.
    • The neurotransmitter and receptor causative in theta have never been clearly determined.
  • Theta in CA3 is much smaller than in CA3:
    • Distal dendritic arbor of CA3 pyramidal cells is considerably smaller than that of CA1 pyramidal neurons.
    • CA3 pyramidal neurons receive perisomatic exitation near their somata from the large mossy terminals of granule cells.
      • Regarding this, size of mossy fiber projection correlates well with spatial ability in mice, possibly causative. link (note: used the dryland radial maze, more appropriate for non-swimming mice!)
    • Intrahippocampal oscillator (CA3?) can change its frequency and phase relatively independently from the extrahippocampal (entorhinal) theta inputs.
  • CA1 interneurons discharge on the descenting phase of theta in the pyramidal cell layer, and are assumed to be responsible for the increased gamma of this phase.
  • CA1 pyramidal cells discharge on the negative phase (makes sense) of theta as recorded from the CA1 pyramidal cell layer.
    • Phase fluctuation of spikesis not random and correlates with behavioral varaibles.
      • Stronger excitation = more spikes earlier in the theta negative phase.
    • Firing of place cells varies systematically with animal position and theta phase -- there is a phase precession.
      • Seems as though place is encoded in both which cell is firing as well as when in theta.
      • alternately, this may be an effect of the CA3 oscillator running slightly faster than the extrinsic oscillator.

Original model for theta oscillation creation (figure 2):

  • Note that all oscillations require a dipole which periodically inverts along it's axis, as is required in a conductive solution.
    • And yet there is no 'null' zone in theta oscillation, as dipole would imply. Rather, there is a gradual shift, more like a traveling wave.
  • Dendrites are passive cables, LFP generated by summed activity of IPSP and EPSP on soma and dendrites.
    • Excitation from perforant path,
    • Inhibition from septum to feed-forward inhibitory neuron inputs.
  • That said, the model is not completely consistent with experimental evidence:
    • The highest probability of discharge in the behaving rat occurs around the positive peak of theta recorded at the level of the distal dendrites, corresponding to the negative phase in the pyramidal level. (Remember, spiking corresponds to sodium influx, hence decreased extracellular +)
    • Cells may oscillate by themselves, without input.
    • The cell connections within the hippocampus matter a lot, too.


  • Induction is present / optimal when the spacing between pulses is 200ms.
    • Priming can be only one pulse!
    • Not clear how this works - endogenous cannabanoids?
  • Theta oscillation may provide a mechanism for bringing together time afferent inducing depolarization and dendritic invasion of fast spikes.


  • A theta cycle may be considered an information quantum, allowing the exchange of information among the linked members in a phase-locked manner. ...
  • This discontinuous mode of operation may be a unique solution to temporally segregate and link neuronal assemblies to perform various operations.
  • Notable support of this hypothesis:
    • Theta cycle phase resets upon sensory stimulation
    • Motor activity can become theta locked.


  • Ketamine blocks NMDA receptors.
  • Granule cells can be eliminated by neonatal X-ray exposure. (why?)

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ref: Weinberger-2009.09 tags: STN DBS PD oscillations beta band review date: 03-05-2012 16:32 gmt revision:5 [4] [3] [2] [1] [0] [head]

PMID-19460368[0] Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?

  • Review of {1075}
  • Suppression of beta-band is correlated with the improvement in combined measures of bradykinesia and rigidity.
    • This does not mean that the oscillations cause rigidity! only that L-DOPA affects both. Focused entirely on Beta band.
  • Previously shown that the degree of beta oscillatory activity in the STN of PD patients correlates with the patients' benefit from dopaminergic medications, but not with baseline motor deficits. (the treatment but not the symptoms)
  • Levy 2000, 2001 for the existence of oscillatory activity in the STN & globus pallidus.
  • Prominent beta band activity in GPi & STN LFP. [Levy 2000, Levy 2001 , Brown 2001]
  • Short train HFS of the STN has been shown to decrease STN-cortex coherence for up to 25s after application. [Wingeier 2006] [Kuhn 2008]
    • Others disagree. [Foffani et al., 2006] and [Rossi et al., 2008] ).
  • In a response task, decrease in beta-band activity negatively correlates with reaction time. [Kuhn 2004]
    • Beta suppression is also correlated with increased motor planning [Williams 2005]
  • Beta band activity also present in healthy monkey striatum, human putamen, and cortex. (I wonder how? many references.)
  • Yet, to date there is no clear evidence that the degree of synchronization in the beta band directly accounts for the motor deficits in PD.
  • It has been recently shown that the percentage of neurons exhibiting oscillatory firing in the beta range correlates well (r squared = 0.62) with the degree by which PD motor symptoms improved after dopamine replacement therapy (Weinberger et al. 2006 PMID-17005611)
  • It should be noted that decrease in beta-band activity may be caused by -- rather than causal of -- decreased akinesia and rigidity.
    • That said, in rats treated with 6-OHDA, an increase in beta band activity took several days to appear after drug administration, and appeared at the same time as clinical symptoms.
  • Interesting! Activity-dependent plasticity was remarkably enhanced with a low dose of levodopa in the basal ganglia output of SNr and that there was a surprisingly good correlation (r squared = 0.81) between symptoms and the level of synaptic plasticity (Prescott et al., 2009) [2].
  • Other theory: exaggerated synchrony in the basal ganglia limits the ability to encode meaningful information, as all neurons are entrained to the same frequency hence undifferentiated.
    • Thought beta band may just be a non-coding resting state. Synaptic plasticity goes awry, and all neurons become entrained. Explains bradykinesia but not rigidity.


[0] Weinberger M, Hutchison WD, Dostrovsky JO, Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?Exp Neurol 219:1, 58-61 (2009 Sep)
[1] Kühn AA, Tsui A, Aziz T, Ray N, Brücke C, Kupsch A, Schneider GH, Brown P, Pathological synchronisation in the subthalamic nucleus of patients with Parkinson's disease relates to both bradykinesia and rigidity.Exp Neurol 215:2, 380-7 (2009 Feb)
[2] Prescott IA, Dostrovsky JO, Moro E, Hodaie M, Lozano AM, Hutchison WD, Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients.Brain 132:Pt 2, 309-18 (2009 Feb)

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ref: Litvak-2011.02 tags: DBS MEG STN synchrony oscillations london connectivity beta basal ganglia date: 02-29-2012 19:59 gmt revision:6 [5] [4] [3] [2] [1] [0] [head]

PMID-21147836[0] Resting oscillatory cortico-subthalamic connectivity in patients with Parkinson’s disease

  • Used MEG plus LFP recordings of the STN.
  • Two spatially and spectrally separated networks were identified.
    • A temporoparietal-brainstem network was coherent with the subthalamic nucleus in the alpha (7-13 Hz) band,
    • whilst a predominantly frontal network was coherent in the beta (15-35 Hz) band.
  • Dopaminergic medication modulated the resting beta network, by increasing beta coherence between the subthalamic region and prefrontal cortex.
  • Idea of characterizing connectivity based on synchronization / comodulation: (Fries 2005).
  • Synchronization is exaggerated in Parkinson's disease (Sharott et al 2005b, Mallet et al 2008).
  • Some patients had dopamine dysregulation syndrome and medication-induced hypersexuality.
  • None of the > 45 Hz STN LFP patterns had a scalp pattern consistent with a cortical source.
  • Cortical source frequency not really that different between ON and OFF medication, except at maybe tremor frequencies.
  • But cortex drives the subthalamic area robustly.
    • That said, these patients were at rest.
    • Small difference between ON and OFF states possibly because they were at rest.
  • Both healthy subjects and those with parkinson's disease show resting connectivity between basal ganglia and the SMA, temporopareital area and parts of the prefrontal cortex. (Postuma and Dagher 2006); Helmich et al 2010).
  • Beta band coupling between cerebral cortex and subthalamic nucleus drops before and during movement (Cassidy et al 2002 PMID-12023312; Lalo et al 2008)
    • During imagination of movement (Kuhn et al 2008).
    • During action observation (Alegre et al 2010).
      • Is this consistent with the conflict / reinforcement learning hypothesis?
  • A big problem is determining if the oscillations are pathological or non-pathological
    • Impossible to control, since we cannot record from healthy humans.


[0] Litvak V, Jha A, Eusebio A, Oostenveld R, Foltynie T, Limousin P, Zrinzo L, Hariz MI, Friston K, Brown P, Resting oscillatory cortico-subthalamic connectivity in patients with Parkinson's disease.Brain 134:Pt 2, 359-74 (2011 Feb)

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ref: -0 tags: distrupted oscillations Mallet 2008 6-OHDA globus pallidus date: 02-29-2012 01:15 gmt revision:5 [4] [3] [2] [1] [0] [head]

PMID-19109506 Parkinsonian beta oscillations in the external globus pallidus and their relationship with subthalamic nucleus activity.

  • Rat 6-OHDA.
  • On rate model: Although synchronization of GP unit activity increased by almost 100-fold during beta oscillations, the mean firing rate of GP neurons decreased compared with controls.
  • Synchronized firing persisted across different brain states, suggesting hardwiring.
  • GP and STN are frequency aligned but phase skewed.
    • Lateral inhibition in GP seems essential / see model.
  • Suggest that GPe / STN could generate oscillations that propagate to the rest of the BG.
    • But then why is the cortex required?

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ref: Mallet-2008.04 tags: DBS oscillations STN beta 6-OHDA rats ECoG acute date: 02-29-2012 01:11 gmt revision:4 [3] [2] [1] [0] [head]

PMID-18448656[0] Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex.

  • STN has pronounced beta band oscillations in PD patients.
  • 6-OHDA rodent model (here) shows the same, depending on state.
    • Synchronization in both local cellular assemblies and broadly across the STN + ECoG.
    • ECoG looks causal in their studies.
    • Frequencies > 15 Hz, not lower (theta), as in other studies.
  • Excessively synchronized beta oscillations reduce the information coding capacity of STN neuronal ensembles, which may contribute to parkinsonian motor impairment.
  • Acute disruption of dopamine transmission in control animals with antagonists of D(1)/D(2) receptors did not exaggerate STN or cortical beta oscillations.
    • This despite the potent agonist induced catalepsy in the rats!
    • Must be neural plasticity & structural.
    • Takes > 4 days.
    • Actual striatal DA levels decrease within 1 h of midbrain 6-OHDA
  • Under normal conditions, beta synchronization may be useful for sensory-motor processing (Uhlhaas and Singer 2006).
  • Synchronized activity is preferentially transmitted due to temporal summation.


[0] Mallet N, Pogosyan A, Sharott A, Csicsvari J, Bolam JP, Brown P, Magill PJ, Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex.J Neurosci 28:18, 4795-806 (2008 Apr 30)

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ref: Timmermann-2003.01 tags: DBS double tremor oscillations DICS beamforming parkinsons date: 02-29-2012 00:39 gmt revision:4 [3] [2] [1] [0] [head]

PMID-12477707[0] The cerebral oscillatory network of parkinsonian resting tremor.

  • Patients had idiopathic unliateral tremor-dominated PD.
  • MEG + EMG -> coherence analysis. (+ DICS for deep MEG recording).
  • M1 correlated to EMG at tremor and double-tremor frequency following medication withdrawal overnight.
    • M1 leads by 15 - 25 ms, consistent with conduction delay.
  • Unlike other studies, they find that many cortical areas are also coherent / oscillating with M1, including:
    • Cingulate and supplementary motor area (CMA / SMA)
    • Lateral premotor cortex (PM).
    • SII
    • Posterior pareital cortex PPC
    • contralateral cerebellum - strongest at double frequency.
  • In contrast, the cerebellum, SMA/CMA and PM show little evidence for direct coupling with the peripheral EMG but seem to be connected with the periphery via other cerebral areas (e.g. M1)
  • Power spectral analysis of activity in all central areas indicated the strongest frequency coherence at double tremor frequency.
    • Especially cerebro-cerebro coupling.
  • These open-ended observation studies are useful!


[0] Timmermann L, Gross J, Dirks M, Volkmann J, Freund HJ, Schnitzler A, The cerebral oscillatory network of parkinsonian resting tremor.Brain 126:Pt 1, 199-212 (2003 Jan)

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ref: -0 tags: oscillations DBS globus pallidus parkinsons date: 02-28-2012 17:24 gmt revision:1 [0] [head]

PMID-17880401 Late emergence of synchronized oscillatory activity in the pallidum during progressive Parkinsonism.

  • In monkeys, progressive dopamine depetion process, recording changes during disease progression -- good!
  • No big change in firing rates, makes sense as this is likely controlled by other network or cellular homeostatic mechanisms.
  • Early in intoxication inhibitory responses to movement disappeared.
    • Yet synchrony did not appear at this time -- it is a sequelae?
    • Correlated activity appeared later, once the animals became severly akinetic.
  • Thus, a causality between the emergence of synchronous oscillations in the pallidum and main parkinsonian motor symptoms seems unlikely.
  • Probably it's movement related activity, not overall states. YES.

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ref: Holgado-2010.09 tags: DBS oscillations beta globus pallidus simulation computational model date: 02-22-2012 18:36 gmt revision:4 [3] [2] [1] [0] [head]

PMID-20844130[0] Conditions for the Generation of Beta Oscillations in the Subthalamic Nucleus–Globus Pallidus Network

  • Modeled the globus pallidus external & STN; arrived at criteria in which the system shows beta-band oscillations.
    • STN is primarily glutamergic and projects to GPe (along with many other areas..)
      • STN gets lots of cortical afferent, too.
    • GPe is GABAergic and projects profusely back to STN.
    • This inhibition leads to more accurate choices.
      • (Frank, 2006 PMID:,
        • The present [neural network] model incorporates the STN and shows that by modulating when a response is executed, the STN reduces premature responding and therefore has substantial effects on which response is ultimately selected, particularly when there are multiple competing responses.
        • Increased cortical response conflict leads to dynamic adjustments in response thresholds via cortico-subthalamic-pallidal pathways.
        • the model accounts for the beneficial effects of STN lesions on these oscillations, but suggests that this benefit may come at the expense of impaired decision making.
        • Not totally convinced -- impulsivity is due to larger network effects. Delay in conflict situations is an emergent property, not localized to STN.
      • Frank 2007 {1077}.
  • Beta band: cite Boraud et al 2005.
  • Huh parameters drawn from Misha's work, among others + Kita 2004, 2005.
    • Striatum has a low spike rate but high modulation? Schultz and Romo 1988.
  • In their model there are a wide range of parameters (bidirectional weights) which lead to oscillation
  • In PD the siatum is hyperactive in the indirect path (Obeso et al 2000); their model duplicates this.


[0] Holgado AJ, Terry JR, Bogacz R, Conditions for the generation of beta oscillations in the subthalamic nucleus-globus pallidus network.J Neurosci 30:37, 12340-52 (2010 Sep 15)

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ref: RodriguezOroz-2001.09 tags: STN SNr parkinsons disease single unit recording spain 2001 tremor oscillations DBS somatotopy organization date: 02-22-2012 18:24 gmt revision:12 [11] [10] [9] [8] [7] [6] [head]

PMID-11522580[0] The subthalamic nucleus in Parkinson's disease: somatotopic organization and physiological characteristics

  • Looks like they discovered exactly what we have discovered ... only in 2001. This is both good and bad.
    • From the abstract: "Neurones responding to movement were of the irregular or tonic type, and were found in the dorsolateral region of the STN. Neurones with oscillatory and low frequency activity did not respond to movement and were in the ventral one-third of the nucleus. Thirty-eight tremor-related neurones were recorded."
  • Again, from the abstract: "The findings of this study indicate that the somatotopic arrangement and electrophysiological features of the STN in Parkinson's disease patients are similar to those found in monkeys."
  • It may be that we want to test differential modulation / oscillation: look for differences between rest and activity, if there is sufficient support for both these in the files we have.
  • These people were much, much more careful about localization of their single-electrode tracks. E.g. they calculated electrode location relative the DBS electrode stereotatically, and referenced this to the postoperative MRI location of the treatment electrode.
  • Many more (32% of 350 neurons) responded to active or passive movement.
  • Of this same set, 15% (31 neurons) had a firing rate with rhythmical activity; 38 neurons had rhythmic activity associated with oscillatory EMG, but most of these were responsive to passive stimulation.
  • Autocorrelation of the neuronal bursting and tremor peaked at mean 7Hz, while autocorr. of EMG peaked at mean 5Hz.
  • This whole paragraph is highly interesting: ''The neuronal response associated with active movements was studied by simultaneous recording of neuronal EMG activity of the limbs. Five tremor-related neurons, recorded while a voluntary movement was performed, were available for analysis. Voluntary activation of a particular limb segment arrested the tremor. This was associated with a change in the discharges of the recorded neuron, which fired at a slower rate and in synchrony with the voluntary movement. On occasions, freezing of the voluntary movement ensued and tremor reappeared, changing the neuronal activity back to the typical 4-5Hz tremor-related activity. The cross-correlation analysis of two such neurons showed a peak frequency of 4.63 and 4.88 Hz for tremor-related activity, and 1.5 to 1.38 Hz during voluntary movement. Whether neuronal discharges in the STN preceded or followed EMG activity of the limbs could not be precisely established under the present conditions.
  • Somatotopic representation in the STN is expected from normal and MTPT-treated monkeys. Indeed, somatotopy is enhanced int he GPm of MTPT-treated monkeys.
    • This somatotopy is likely to result from organized afferent from the primary motor cortex (M1) to dorsolateral STN; this is the target of DBS treatment. Ventral and medial STN seems to project to associative and limbic cortical regions.
    • It seems they think the STN is generally not diseased, it is just a useful target for stimulating without evoked movement as in M1. This is consistent with optogenetic studies by Deisseroth [1].
    • Supporting this: "DBS of STN in Parkinson's disease improves executive motor functions, but aggravates conditional associative learning.
  • Interesting: In Parkinson's disease patients with tremor, Levy and colleagues found synchronization and a high firing rate (>10Hz) while recording pairs of neurons >600um apart.
  • Recordings of cortical activity through EEG and STN LFP showed significant coherence in the beta and gamma frequency bands during movement - consistent with corticosubthalamic motor projection. ... and suggest that the STN neurons involved in parkinsonian tremor are the same as the ones ativated during the performance of a voluntary movement. (! -- I agree with this.)
  • More: The reciprocal inhibitory-excitatory connections tightly linking the GPe and the STN may generate self-perpetuating oscillations.

Old notes:

  • this paper concentrates on STN electrophysiology in PD.
    • has a rather excellent list of references.
  • found a somatotopic organization in the STN, with most motor-related units more irregular and in the dorsolateral STN.
  • found a substantial fraction of tremor-synchronized neurons.
  • conclude that the somatotopic organization is about the same as in monkeys (?) (!)
  • M1 projects to STN, as verified through anterograde tracing studies. [1] These neurons increase their firing rate in response to passive movements.
  • there appears to be a relatively-complete representation of the body in the dorsolateral STN.


[0] Rodriguez-Oroz MC, Rodriguez M, Guridi J, Mewes K, Chockkman V, Vitek J, DeLong MR, Obeso JA, The subthalamic nucleus in Parkinson's disease: somatotopic organization and physiological characteristics.Brain 124:Pt 9, 1777-90 (2001 Sep)
[1] Gradinaru V, Mogri M, Thompson KR, Henderson JM, Deisseroth K, Optical deconstruction of parkinsonian neural circuitry.Science 324:5925, 354-9 (2009 Apr 17)

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ref: Levy-2002.06 tags: DBS parkinsons STN oscillations beta date: 02-22-2012 18:17 gmt revision:4 [3] [2] [1] [0] [head]

PMID-12023310[0] Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.

  • Key finding: Synchronized HFOs (high-frequency oscillations, 15-30Hz here) between STN neurons were observed in 28 out of 37 pairs in five patients who had tremor in the operating room and none of 45 pairs in three patients who did not.
  • Active movement suppressed synchronized HFOs in three out of five pairs of neurones, independent of changes in firing rate.
  • Dopamine treatment also supressed LFP HFOs, synchrony between STN neuron pairs, and synchrony between tremor cells.
  • They suggest that STN is diseased ... however, STN does not receive a great number of SNc projections, hence the pathology may merely bre reflective of upstream structures.


[0] Levy R, Ashby P, Hutchison WD, Lang AE, Lozano AM, Dostrovsky JO, Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.Brain 125:Pt 6, 1196-209 (2002 Jun)

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ref: Cassim-2002.12 tags: DBS STN oscillations ablation france VIM amish. date: 02-22-2012 16:59 gmt revision:6 [5] [4] [3] [2] [1] [0] [head]

PMID-12495873[0] Relationship between oscillations in the basal ganglia and synchronization of cortical activity.

  • STN neurons in the rat typically fire in + phases of cortical EEG.
  • Ablation of ipsilateral cortex makes firing random
  • 6-OHDA animals the orignial busting pattern is increased;
  • ablation of the cortex makes the firing pattern tonic.
  • GP firing in parkinsonian animals become very oscillatory as opposed to movement-locked.
  • Levy et al 2000 -- STN neurons show both oscillatory behavior and tremor-locked behavior, and some both.
  • with DBS, dominant EMG frequency shifts from ~ 12 Hz to ~40 Hz piper rhythm.
  • Reiterate that Beta rhythms occur not during movement, but only during tonic or sustained forces. Oscillations could be a means of keeping a 'symbolic' movement alive.
    • Therefore, it is possible to find EEG-EEG coherence between two distant cortical entities involved in the same motor task.
      • Really need to record LFP during DBS surgeries.
  • It should be kept in mind that the VIM has no direct relationship with the basal ganglia, and is rather involved in the cerebellar system and the cortico-ponto-cerebellothalamo-cortical loop. (cortex, pontine nucleus, cerebellum / thalamic cerebellum, cortex)
  • Reiterate the importance of > 60Hz oscillations in STN and GPi.
    • the authors put forward the hypothesis of two systems within the basal ganglia: a "low-frequency system" and a "high-frequency system". The "low-frequency system" would impair movement, and would be blocked either by dopaminergic stimulation or focal destruction of GPI or STN, thus explaining the good results of pallidotomy for example. The "high-frequency system" would promote movement, and would be artificially enhanced by high frequency stimulation of either nucleus.
  • Basal ganglia oscillations within the beta band were recently demonstrated to be reduced by voluntary movement [53].

Also, random: the world's highest rate of Parkinson's disease is in the Amish in the NE US. More than twice that of anywhere else; http://www.viartis.net/parkinsons.disease/news/090801.htm


[0] Cassim F, Labyt E, Devos D, Defebvre L, Destée A, Derambure P, Relationship between oscillations in the basal ganglia and synchronization of cortical activity.Epileptic Disord 4 Suppl 3no Issue S31-45 (2002 Dec)

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ref: Brown-2003.04 tags: PD oscillations DBS date: 02-22-2012 16:06 gmt revision:4 [3] [2] [1] [0] [head]

PMID-12671940[0] Oscillatory nature of human basal ganglia activity: relationship to the pathophysiology of Parkinson's disease.

  • Break oscillations into > 30 Hz and < 60 Hz bands.
    • these two are inversely affected by movement, and inversely affected by dopamine treatment.
    • This seems inconsistent with the other literature. (?)
  • Lesions of the GPi improve dyskinesias, without deleterout effects on motor function.
  • The tact assumption from the MPTP monkey research is that synchronization and bursting is an abnormal phenomena.
    • Also suggest that synchronization may be a means of 'binding' or increasing the salience of input.
  • The degree of synchronization increases during non-oscillating periods in PD patients treated with the dopamine agonist apomorphine.
  • [27] PMID-11431506 and there is one report of locking in patients without tremor.
    • In both nuclei, APO increased the overall proportion of spikes in burst discharges (as detected with Poisson "surprise" analysis), and a greater proportion of cells with an irregular discharge pattern was observed.
    • During the OFF state, more than 15% of neurons tested (STN = 93, GPi = 63) responded to passive movement of two or more joints. After APO, this proportion decreased significantly to 7% of STN cells and 4% of GPi cells (STN = 28, GPi = 26).
    • Concurrent with a reduction in limb tremor, the percentage of cells with tremor-related activity (TCs) was found to be significantly reduced from 19 to 6% in the STN and 14 to 0% in the GPi following APO administration.
  • [31] PMID-9990083 there is evidence that human STN and GPi units firing at tremor frequency show only transient periods of locking to peripheral tremor
    • We found that GPi tremor-related activity at a given site could fluctuate between states of synchronization and independence with respect to upper limb tremor. Consistent with this finding, some paired recording sites within GPi showed periods of transient synchronization. These observations support the hypothesis of independent tremor-generating circuits whose coupling can fluctuate over time.
  • Monkeys treated with MPTP show pronounced increases in synchrony at < 30 Hz.
  • Levodopa markedly increases > 60 Hz coherence between GP & midline EEG.
    • "The synchronization of single units in STN or GPi at high frequencies has not been demonstrated in microelectrode studies to date. (2002).
    • HF coherence is found between SNT and GPi, and these structures w SMA.
  • Stimulation of the pallidium and enteopeduncular nucleus in cats at 3-10Hz leds to synchronization of the EEG and gradual slowing and eventual cessation of spontaneous movements.
    • Could this abnormal, low-frequency, synchronous oscillatory activity in GPi and its input STN act, by means of the thalamus, to hold the motor cortex in a low-frequency antikinetic state in Parkinson’s disease? [7].
  • There is a disappearance of > 60 Hz oscillations in the STN with drowsiness [29].
  • Complex movements are particuarly difficult for PD patients.
  • Human GPi neurons normally fire at 85 to 140 Hz -- so 130 Hz stimulation may entrain them.

Conclusion: he really thinks that there is a strong dichotomy between HF, pro-kinetic, and MF, anti-kinetic oscillations.


[0] Brown P, Oscillatory nature of human basal ganglia activity: relationship to the pathophysiology of Parkinson's disease.Mov Disord 18:4, 357-63 (2003 Apr)

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ref: Bevan-2002.1 tags: STN GPe globus pallidus oscillations parkinsons DBS date: 02-22-2012 15:13 gmt revision:8 [7] [6] [5] [4] [3] [2] [head]

PMID-12220881[] Move to the rhythm: oscillations in the subthalamic nucleus-external globus pallidus network.

  • !!! autonomous oscillation of STN and GPe underlies tonic activity and is important for synaptic activity (e.g. normal??)
    • this is a review, of course.
  • during quiet wakefulness, neurons in STN and GPe fire differently without rhythm or strong correlation.
    • this is more pronounced when STN/GPe neurons are isolated from synaptic input (e.g. when prepared in a slice)-- they have inherent oscillatory characteristics. hum.
      • this may allow persistent activity or timed (gating) of planned activity (as opposed to timing of compensatory movement, which are mostly handled by the cerebellum).
      • the persistent activity must be more complicated than synchronized firing as in PD.
      • Random thought: I wonder if you 'clocked' the brain you would get discrete reaction times. Longshot; would need to review up and down states in the cortex?
  • during voluntary movement, GPe and STN neurons display a complex relationship to features of motor activity.
  • GPe and STN are reciprocally connected (STN with the Glu, GPe with the GABA)
    • as in other original papers, most of the axons from these regions have branched axons that mediate both reciprocal connections and innervation of output nuclei.
  • interesting thought: STN/GPe network could act as a 'generic' recursive pattern generator.
  • see figure 1 - single IPSP regulate the timing of spikes in the STN. large IPSP can synchronize and entrain the intrinsic high firing rate of STN neurons by prolonging the interspike interval.
    • bursts of IPSP can lead to rebound excitation, and hence a paradoxical increase in activity inn the STN. PMID-11877509[]
      • large IPSPs reset STN neurons oscillatory cycle & lead to synchronization
      • small IPSPs lead to phase-dependent delays and probably lead to desynchronization.
      • neuromodulators, like ACh, serotonin, and dopamine, can influence the polarization of STN neurons, and hence will have a profound effect on activity.
      • STN activity is more dependent one the pattern of afferent activity (of course!) than the gross magnitude of incoming spikes.
  • figure 2 - the network configuration between STN and GPe can markedly affect resulting activity. When there are possible reciprocal connections, the network produces tremor; when the network is more organized so that STN cannot recurrently activate GPe, multiple rhythms occur.
    • recall that both structures have extensive & sparsely connected dendritic fields, and are highly topographically organized.
  • figure 3 - [2,3]- oscillatory activity in the STN is a consequence of dopamine depletion and is also a feature of normal activity.
    • this is dependent on the presence of cortex. lack of cortex = regular firing.
    • GPe firing is tonic and constant in normal animals, and becomes oscillatory in 6-OHDA treated animals.
  • administration of dopamine agonists in PD patients causes higher frequency rhythms (30-70hz); without treatment, oscillations are in the 8-12 and lower range.

my notes:

  • IPSPs seem to have a very interesting and complex effect on the firing properties of tonically-active STN nenurons. who knows how this is being used, and in what representation the associated information is being processed?
  • still need to understand what dopamine is doing, and why absence leads to oscillations!
    • dopamine must modulate basal ganglia insensitivity to cortex.


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ref: -3000 tags: DBS STN oscillations beta gamma research date: 02-21-2012 16:51 gmt revision:22 [21] [20] [19] [18] [17] [16] [head]

There seems to be an interesting connection between excessive grip force, isometric muscle contraction causing coherence between motor cortex and EMG, lack of inhibition on delayed response and go-no-go task, and experiments with STN lesioned rats, and the high/low oscillation hypothesis. Rather tenuous, I suppose, but let me spell it out. ( My personal impression, post-hoc, is that this is an epiphenomena of something else; evidence is contradictory.)

  1. PD patients, STN DBS impairs ability to match force characteristics to task requirements both in terms of grip force {88}, and when lifting heavy and light objects {88-2}. This is consistent with GPi function controlling the vigor or scaling of muscle responses
  2. Isometric force creation frequently engages the piper rhythm between cortex and muscles {1066}, which may be a means of preserving motor state {1066-4}.
  3. In PD patients there is marked increase in beta oscillation and synchronization {1064}, which decreases during movement {829}. Some suggest that it may be a non-coding resting state {969}, though beta-band energy is correlated with PD motor symptoms PMID-17005611, and STN DBS attenuates the power in the beta band {710-2},{753},{1073}, and DCS is likely to do the same PMID-21039949. Alternatively synchrony limits the ability to encode meaningful information. The beta band activity does not seem associated with rest tremor {1075}. Furthermore, beta band decreases prior and during movement, and with the administration of levodopa oscillation shifts to higher frequency -- the same frequency as the piper rhythm {1075}. Closed-loop stimulation with a delay (80ms) designed to null the beta oscillations is more effective than continuous high frequency DBS {967}.
  4. PD patients have deficits in inhibition on go-no-go and delayed response tasks that is exacerbated by STN DBS {1077-3}, as well as expedited decision making in conflict situations {1077} Lesioning the STN in rats has similar effect on delayed reward task performance, though it's somewhat more complicated. (and their basal ganglia is quite a bit different). {677}.
  5. The <30 Hz and >30Hz bands are inversely affected by both movement and dopamine treatment. {1069}

footnote: how much is our search for oscillations informed by our available analytical techniques?

Hypothesis: Impulsivity may be the cognitive equivalent of excess grip force; maintenance of consistent 'force' or delayed decision making benefits from Piper-band rhythms, something which PD abolishes (gradually, through brain adaptation). DBS disrupts the beta (resting, all synchronized) rhythm, and thereby permits movement. However it also effectively 'lesions' the STN, which leads to cognitive deficits and poor force control. (Wait .. DBS plus levodopa improves 40-60Hz energy -- this would argue against the hypothesis. Also, stroke in the STN in normal individuals causes hemiballismus, which resolves gradually; this is not consistent with oscillations, but rather connectivity and activity.)

Testing this hypothesis: well, first of all, is there beta-band oscillations in our data? what about piper band? We did not ask the patients to delay response, so any tests thereof will be implicit. Can look at relative energy 10Hz-30Hz and 30Hz-60Hz in the spike traces & see if this is modulated by hand position. (PETH as usual).

So. I made PETHs for beta / gamma power ratio of the spiking rate, controlled by shuffling the PETH triggers. Beta power was between 12 and 30 Hz; gamma between 30 and 75 Hz, as set by a noncausal IIR bandpass filter. The following is a non-normalized heatmap of all significant PETHs over all sessions triggered when the hand crossed the midpoint between targets. (A z-scored heatmap was made as well; it looked worse).

X is session number, Y time, 0 = -1 sec. sampling rate = 200 Hz. In one file (the band) there seems to be selective gamma inhibition about 0.5 sec before peak movement. Likely it is an outlier. 65 neurons of 973 (single and multiunits together) were significantly 'tuned' = 6.6%; marginally significant by binomial test (p=0.02). Below is an example PETH, with the shuffled distribution represented by mean +- 1 STD in blue.

The following heatmap is created from the significant PETHs triggered on target appearance.

80 of the 204 significant PETHs are from PLEX092606005_a. The total number of significant responses (204/1674, single units and multiunits) is significant by the binomial test p < 0.001, with and without Sept. 26 removed. Below is an example plot (092606005). Looks pretty damn good, actually.

Let's see how stable this relationship is by doing a leave-half out cross-validation, 10 plies, in red below (all triggers plotted in black)

Looks excellent! Problem is we are working with a ratio, which is prone to spikes. Fix: work in log space.

Aggregate response remains about the same. 192 / 1674 significant (11.5%)

In the above figure, positive indicates increased β\beta power relative to γ\gamma power. The square shape is likely relative to (negative lags) hold time and (positive lags) reaction time, though the squareness is somewhat concerning. Recording is from VIM.

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ref: notes-3000 tags: darpa 2007 misha report oscillations old notes date: 02-16-2012 17:50 gmt revision:7 [6] [5] [4] [3] [2] [1] [head]

We have found the following types of neurons during acute intraoperative recrodings from the subthalamic nucleus (STN) of awake parkinson's patients. During the surgeries the patients opened and closed their hand, instrumented through a virtual-reality data glove, in order to move a cursor to randomly presented targets in a 1-dimensional field.

It is thought that the STN controls the gating and timing of movements, and this gate/relay is implicated in the pathological oscillatory loop seen in Parkinson's disease. Therefore, it is not surprising that we have found cells that are tuned to both movement initiation and simultaneously tuned to oscillatory features of the behavior.

Below the probability of firing, (red = high, blue = low) is plotted vs time (x-axis) and y (target gating signal). The target gating signal is 1 400 ms around the appearance of a new target to the right of the cursor, -1 when the target appears to the left of the cursor, and 0 everywhere else; 1 corresponds to the top of the graph, and -1 to the bottom. This probability was caluclated in sliding 50ms lags across the x axis to illuminate any fixed temporal relationships; that is, if a neuron had a high probability of firing 500 ms before target appearance, the image would be red @ a lag of 0.5 (on the x axis) and 1 on the y axis. This method is a nonparametric, minimal-assumption way of looking at the correlations between behavior and neural firing. It is only assumed that the relationship between neural firing times and behavior is stationary, e.g. it does not evolve with time; this is a relatively safe assumption given the recording are generally short.

This plot shows a neuron which fires preferentially when a target appears and the patient moves to the left (again, in this graph: y = -1 indicates target appears to the left, + 1 target to the right, and 0 otherwise). Note that there is noticable oscillations, due to the fact that the patient's behavior was very periodic, with a period of around 2 seconds. The neuron was inhibited around the instant of target apperance, independent of direction, as indicated by the blue regions at y = -1 and 1 around lag 0.

This plot shows a neuron which is inhibited just before target apperance (in this plot, y = 1 400ms around target appearance, independent of direction). That is, the neuron stops firing upon sucessful completion of a movement. This neuron shows no pathological oscillatory tuning; therefore, it might be assumed that not all of the STN is incapacitated by Parkinson's disease.

Here is another example of a neuron that does not show oscillatory firing behavior. In this graph, y = 1 when the patient is opening or closing his hand (equivalently the cursor velocity exceeds a threshold); y = 0 otherwise. This neuron is therefore inhibited during periods of movement. Note that around a lag of 2.5 seconds, the neuron has a higher probability of firing (the red region), possibly indicating positive firing upon successful completion of a movement.

Another example of a neuron that is tuned to thresholded cursor velocity, though this time, the firing rate becomes positive just around the instant of movement. Note here there is evidence of highly periodic behavior, as seen in the green/yellow regions spaced about 1.6 seconds apart along y=1. The region at lag = 1.6 secons corresponds to the movement following target acquisition, hence exhibits a higher firing rate.

This neuron, like the one above, fires strongly whenever the hand moves. Interestingly, there appeared to be no directional information in either of these cells.

Finally, we discovered that there appears to be error-correlated firing within the STN. The neuron shown above is selectively inhibited around periods where the cursor and target positions differ. In the plot above y=1 indicates the absolute value of the target position - the cursor position exceeds a threshold of 20% of the total range (this is subtly different from the target apperance signal, as the patient can over shoot or under shoot the target position with the cursur, upon which this signal will be 1.

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ref: Berke-2009.09 tags: DBS oscillations high gamma synchronization date: 02-16-2012 17:48 gmt revision:1 [0] [head]

PMID-19659455[0] Fast oscillations in cortical-striatal networks switch frequency following rewarding events and stimulant drugs.

  • 50 Hz resting rhythm in the straitum is coherent with the piriform cortex;
  • Striatum synchronizes with the frontal cortex at 80-100 Hz following reward or amphetamine administration.
  • Switching between discrete oscillatory states may allow different modes of information processing during decision-making and reinforcement-based learning, and may also be an important systems-level process by which stimulant drugs affect cognition and behavior.


[0] Berke JD, Fast oscillations in cortical-striatal networks switch frequency following rewarding events and stimulant drugs.Eur J Neurosci 30:5, 848-59 (2009 Sep)

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ref: Chan-2011.01 tags: GPi DBS burst oscillations date: 01-26-2012 17:29 gmt revision:1 [0] [head]

PMID-20727974[0] Bursts and oscillations as independent properties of neural activity in the parkinsonian globus pallidus internus.

  • 132 GPi cells in 14 Parkinson's disease patients
  • segregated into oscillatory and non-oscillatory cells.
    • No significant difference in burstiness between the two.
    • Except for oscillatory cells in the alpha region (8-13Hz), which were burstier than other cells.
  • conclusion: busrting and oscillations may be caused by different things.


[0] Chan V, Starr PA, Turner RS, Bursts and oscillations as independent properties of neural activity in the parkinsonian globus pallidus internus.Neurobiol Dis 41:1, 2-10 (2011 Jan)

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ref: Brown-2001.12 tags: EMG ECoG motor control human coherence dopamine oscillations date: 01-19-2012 21:41 gmt revision:5 [4] [3] [2] [1] [0] [head]

PMID-11765129[0] Cortical network resonance and motor activity in humans.

  • good review.
  • No coherence between ECoG and eMG below 12 Hz; frequency coherence around 18 Hz.
    • This seen only in high-resolution ECoG; lower resolution signals blurs the sharp peak.
  • Striking narrowband frequency of coherence.
  • ECoG - ECoG coherence not at same frequency as EMG-ECoG.
  • Marked task-dependence of these coherences, e.g. for wrist extension and flexion they observed similar EMG/ECoG coherences; for different tasks using the same muscles, different patterns of coherence.
  • Pyramidal cell discharge tends to be phase-locked to oscillations in the local field potential (Murthy and Fetz 1996)
    • All synchronization must ultimately be through spikes, as LFPs are not transmitted down the spinal cord.
  • Broadband coherence is pathological // they note it occurred during cortical myclonus (box 2)
  • Superficial chattering pyramidal cells (!!) firing bursts of frequency at 20 to 80 Hz, interconnected to produce spike doublets (Jefferys 1996).
  • Dopamine restores coherence between EMG and ECoG in a PD patient.


[0] Brown P, Marsden JF, Cortical network resonance and motor activity in humans.Neuroscientist 7:6, 518-27 (2001 Dec)

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ref: Hagbarth-1983.02 tags: piper rhythm oscillations feedback proprioception spinal reflex date: 01-19-2012 21:41 gmt revision:2 [1] [0] [head]

PMID-6869036[0] The Piper rhythm--a phenomenon related to muscle resonance characteristics?

  • Piper rhythm: the tendency towards rhytmical 40-60 Hz grouping of motor unit potentials in steadily contracting human muscles.
  • Recording of nerves in muscles did not support the idea that the Piper rhythm is dependent on afferent spindle pulses causing reflex entrainment. (loop too slow).
  • TThis wouldn't make sense anyway, as the same rhythm appears in different muscles with markedly different mechanical properties.
  • Likkely cause is the cerebrum, upper oscillations. Interesting!
  • See also: PMID-9862895[1] Cortical correlate of the Piper rhythm in humans.
    • MEG data is consistent with the cortex being the origin of the Piper rhythm.
  • And PMID-10203308[2] Rhythmical corticomotor communication.
    • The rhythmic modulation may form a tool for efficient driving of motor units but we express some reservations about the assumed binding and attention-related roles of the rolandic brain rhythms.
  • PMID-10622378[3] Cortical drives to human muscle: the Piper and related rhythms.
    • Alternately, oscillations may be a form of holding state.
    • They think gamma frequencies are a means of binding together simultaneously activated isometric muscles.
    • Inadequate output from the basal ganglia leads to a disappearance of the beta and piper drives to muscle.
    • Did we see and piper band osc activity? Did not look.


[0] Hagbarth KE, Jessop J, Eklund G, Wallin EU, The Piper rhythm--a phenomenon related to muscle resonance characteristics?Acta Physiol Scand 117:2, 263-71 (1983 Feb)
[1] Brown P, Salenius S, Rothwell JC, Hari R, Cortical correlate of the Piper rhythm in humans.J Neurophysiol 80:6, 2911-7 (1998 Dec)
[2] Hari R, Salenius S, Rhythmical corticomotor communication.Neuroreport 10:2, R1-10 (1999 Feb 5)
[3] Brown P, Cortical drives to human muscle: the Piper and related rhythms.Prog Neurobiol 60:1, 97-108 (2000 Jan)

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ref: Levy-2002.04 tags: DBS oscillations synchrony date: 01-19-2012 21:00 gmt revision:1 [0] [head]

PMID-11923450[0] Synchronized neuronal discharge in the basal ganglia of parkinsonian patients is limited to oscillatory activity.

  • simultaneous recording for pallidotomy or STN DBS.
  • In the five pallidotomy patients without limb tremor during the procedure, none of the 73 GPi pairs and 15 GPe pairs displayed synchronous activity. we got the same result
  • In the three pallidotomy patients with limb tremor, 6 of 21 GPi pairs and 5 of 29 GPe pairs displayed oscillatory synchronization in the frequency range of the ongoing limb tremor (3-6 Hz) or at higher frequencies (15-30 Hz).
  • Synchronized activity was not observed in the SNr (10 pairs).


[0] Levy R, Hutchison WD, Lozano AM, Dostrovsky JO, Synchronized neuronal discharge in the basal ganglia of parkinsonian patients is limited to oscillatory activity.J Neurosci 22:7, 2855-61 (2002 Apr 1)

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ref: Eusebio-2009.05 tags: DBS STN beta gamma oscillations synchrony tremor review date: 03-23-2009 18:32 gmt revision:1 [0] [head]

PMID-19233172[0] Synchronisation in the beta frequency-band - The bad boy of parkinsonism or an innocent bystander?

  • Excessive synchronisation of basal ganglia neuronal activity in the beta frequency band has been implicated in Parkinson's disease
  • However, the extent to which beta synchrony has a mechanistic (rather than epiphenomenal) role in parkinsonism remains unclear, and the suppression of this activity by deep brain stimulation is contentious.
PMID-16289053[1] Intra-operative STN DBS attenuates the prominent beta rhythm in the STN in Parkinson's disease.
  • Beta rhythm for them = 11-30Hz. Observed in the LFP recorded from the DBS electrode itself.
  • This study shows for the first time that STN DBS attenuates the power in the prominent beta band recorded in the STN of patients with PD.


[0] Eusebio A, Brown P, Synchronisation in the beta frequency-band - The bad boy of parkinsonism or an innocent bystander?Exp Neurol no Volume no Issue no Pages (2009 Feb 20)
[1] Wingeier B, Tcheng T, Koop MM, Hill BC, Heit G, Bronte-Stewart HM, Intra-operative STN DBS attenuates the prominent beta rhythm in the STN in Parkinson's disease.Exp Neurol 197:1, 244-51 (2006 Jan)