NeuroTalk Support Groups - DBS (Deep Brain Stimulation) for RSD and Dystonia

From Hi (sorry, this has become very long) http://neurotalk.psychcentral.com/thread130082.html

Dear frogga, Sarah Mae, Ali and Allen -

Once more, I bow my head to true heroes who have for too long endured the horrors of the worst of RSD or just plain old neuropathic pain (NPP). And congratulations to one and all that retain the intellectual faculties and discipline to get a degree through all of this! (For me, I seem to be “parallel processing” a myriad of tasks into simultaneous incompletion.)

But frogga's reference to DBS brings to mind the most important article I've read in years, Abnormal thalamocortical activity in patients with Complex Regional Pain Syndrome (CRPS) Type I, Walton KD, Dubois M, Llinás RR, Pain 2010 Jul;150(1):41-51, Epub 2010 Mar 24 FULL TEXT @ http://www.rsds.org/2/library/articl..._Pain_2010.pdf:

Dept. of Physiology & Neuroscience, New York University School of Medicine, 550 First Ave., New York, NY 10016, USA.

Abstract
Complex Regional Pain Syndrome (CRPS) is a neuropathic disease that presents a continuing challenge in terms of pathophysiology, diagnosis, and treatment. Recent studies of neuropathic pain, in both animals and patients, have established a direct relationship between abnormal thalamic rhythmicity related to Thalamo-cortical Dysrhythmia (TCD) and the occurrence of central pain. Here, this relationship has been examined using magneto-encephalographic (MEG) imaging in CRPS Type I, characterized by the absence of nerve lesions. The study addresses spontaneous MEG activity from 13 awake, adult patients (2 men, 11 women; age 15-62), with CRPS Type I of one extremity (duration range: 3months to 10years) and from 13 control subjects. All CRPS I patients demonstrated peaks in power spectrum in the delta (<4Hz) and/or theta (4-9Hz) frequency ranges resulting in a characteristically increased spectral power in those ranges when compared to control subjects. The localization of such abnormal activity, implemented using independent component analysis (ICA) of the sensor data, showed delta and/or theta range activity localized to the somatosensory cortex corresponding to the pain localization, and to orbitofrontal-temporal cortices related to the affective pain perception. Indeed, CRPS Type I patients presented abnormal brain activity typical of TCD, which has both diagnostic value indicating a central origin for this ailment and a potential treatment interest involving pharmacological and electrical stimulation therapies. Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

PMID: 20338687 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/20338687

Before going further, I should note that Rodolfo Llinás, the senior and corresponding author, Department Chairman and Professor of Physiology and Neuroscience at the New York University School of Medicine, is widely regarded ''one of the great neuroscientists of the age.'' Listening to the Conversation of Neurons (Scientist at Work: Dr. Rodolfo Llinas), Philip J. Hilts, New York Times, May 27, 1997 http://www.nytimes.com/1997/05/27/sc...f-neurons.html:

''We think about the brain differently as a result of him,'' Dr. [Roger] Traub , a neuroscientist at I.B.M.'s laboratories in Yorktown Heights, N.Y., said. ''Some people do beautiful cell work in the laboratory. Others are great thinker-types. There are not many people who do both, and Llinas is one.''

And that was before Dr. Llinás delivered his seminal paper on thalamo-cortical oscillations before the annual meeting of The Society for Neuroscience in October, 1999. New Way Of Looking At Diseases Of the Brain, Sandra Blakeslee, New York Times, October 26, 1999 http://www.nytimes.com/1999/10/26/sc...the-brain.html Because of the beautiful manner in which the theory is explained in lay terms, I cannot recommend the article highly enough, where “Abnormal thalamocortical activity in patients with Complex Regional Pain Syndrome (CRPS) Type I” can be tough sledding in places. And A Pro Pos of frogga’s wait-list for DBS, the NYT article concludes with the following:

All these disorders might be treated by implanting electrodes into the thalamus to break the abnormal oscillation patterns, Dr. Llinas said. In fact, the most effective treatment for Parkinson's patients who do not respond to drug therapy involves putting electrodes directly into the thalamus. ''This breaks the abnormal disconnection and the person immediately gets better,'' Dr. Llinas said. ''But you have to keep the electrode in. It's like a pacemaker.'' Similar surgeries have been tried successfully for chronic pain and depression. In each case, the electrode is targeted on only a few thousand cells.

Presumably, the NY Times article was based upon the October 21, 1999 paper published (with a considerable amount of math) as Thalamocortical dysrhythmia: A neurological and neuropsychiatric syndrome characterized by magnetoencephalography, Llinás RR, Ribary U, Jeanmonod D, Kronberg E, Mitra PP, Proc Natl Acad Sci U S A 1999 Dec 21; 96(26):15222-7 FULL TEXT @ http://www.pnas.org/content/96/26/15222.full.pdf

Department of Physiology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.

Abstract
Spontaneous magnetoencephalographic activity was recorded in awake, healthy human controls and in patients suffering from neurogenic pain, tinnitus, Parkinson's disease, or depression. Compared with controls, patients showed increased low-frequency theta rhythmicity, in conjunction with a widespread and marked increase of coherence among high- and low-frequency oscillations. These data indicate the presence of a thalamocortical dysrhythmia, which we propose is responsible for all the above mentioned conditions. This coherent theta activity, the result of a resonant interaction between thalamus and cortex, is due to the generation of low-threshold calcium spike bursts by thalamic cells. The presence of these bursts is directly related to thalamic cell hyperpolarization, brought about by either excess inhibition or disfacilitation. The emergence of positive clinical symptoms is viewed as resulting from ectopic gamma-band activation, which we refer to as the "edge effect." This effect is observable as increased coherence between low- and high-frequency oscillations, probably resulting from inhibitory asymmetry between high- and low-frequency thalamocortical modules at the cortical level.

PMID: 10611366 [PubMed - indexed for MEDLINE] PMCID: PMC24801

http://www.ncbi.nlm.nih.gov/pubmed/10611366 (Cited by an astoundingly high 35 PubMed Central articles.)

But where it gets cool, is that Dr. Llinás isn’t necessarily speaking in terms of the implantation of electrodes through conventional neurosurgery. See, Transcript, “Enter the 'i of the vortex'” with neuroscientist Rodolfo - Llinás [The Science Studio] April 17, 2007, from the apparently uncopyrighted transcript of an interview which is itself designed to be freely linked to any website, http://thesciencenetwork.org/program...-of-the-vortex:

BINGHAM: What about this new work you’ve been doing, using… Can you explain this new work you’ve been doing using nanowires? “Nano” of course is very much a buzz phrase and perhaps you could explain that we’re just talking about extremely small technology here and how it works and so on?

LLINÁS: It is something that is the obvious next step in the conversation we’ve been having. We were saying look, the nervous system evolved to move, intelligent language, and all the things are pre-motor events that allow you to then move intelligently. Moving intelligence is what we do at this point and we extend that. We also know these things can be modulated by electrical means. You can stimulate, you can move your foot, you can stimulate and get someone who has a disease to not have the disease anymore and so on. So the system is amenable to direct interaction with the external world by means other than nerves. Comma oh my god, closed parentheses, really. And I say yeah. The problem is that the brain is guarded by bone.

I say in the book [I of the Vortex: From Neurons to Self (2002)] we have an exoskeleton when we talk about the brain. The rest, the muscles are out and so on, so ok. If a) the brain were to, if the cranium were to be transparent, we could see the activity of the brain, instead of looking at people’s faces, you would look at people’s brains and say don’t think that. You could see the patterns and say no, no, don’t take it like that. The same thing happens when somebody tells you that they’re not agreeing with you.

Imagine that in addition to doing like that, you could say well what if I actually communicate with you directly so we don’t have to go through all this blabbering or this talking and I’ll tell you exactly how I feel. How could I do it in principle? Well I could go directly to the brain. The problem is, oh my god, but you have to then penetrate this bone. So thinking about how could we do it, is well, the brain is full of holes, don’t make any new ones. And what are the holes I’m thinking about? The vascular system. So imagine. The blood vessels, right. Imagine yourself becoming very small in this beautiful whole film- science fiction, into the vessels and you go into the brain. Where can you go? Anywhere. The brain is completely vascularized. It’s full of these vessels and they occur every 15 microns, it’s a 3-dimensional scaffolding that goes everywhere. And then the question is, don’t go to the brain through the outside, go to the brain through the inside. Why not put a wire up to anywhere you want in the brain and try to record or stimulate or both. But it has to be a very thin wire because you don’t want it to bother circulation. It has to be of such material that it’s not recognized by the body as being there. Can this be done? The answer is yeah, there are ways to protect the wire from being…

BINGHAM: You’re right, this does sound like science fiction and the utility would be what?

LLINÁS: The utility would be…. The utility would be as follows. At this moment we are getting to about a 30 nanometer wire. It is a third of a micron- a micron being very small- thousandths of a millimeter. You can put several hundred in the diameter of a single hair. Ok so you float this thing, say you want to do more than one, you want to do ten or a hundred or a thousand or ten thousand or however many, so you can wire the brain from the inside. What can you do? Two things, you can record and you can stimulate. Ok so you have something in front of you about your brain or in front of you about somebody else’s brain, heaven forbid, with the ability to address the brain. What is the first thing you do? Well you probably instead of doing electrical stimulation of the top, you’ll do it to the vessel.

Now is this done? The answer is, it is done every day in neurosurgery for other
reasons. The people who do that are called interventional neuroradiologists and they put in things that go around and let go little objects that would close a vessel that has an aneurysm or something. You correct, this is things that people know how to do very well and I have many friends who are neuroradiologists. You say, ok can you put this thing and please I’d like to have my visual cortex wired. Yeah sure. Put it in. You put a little ball of these wires which then on touching fluid begin to slowly move out and of course you wire part of the brain. They are so small they are not going to impede circulation; they are not going to produce coagulation. They are simply not going to be recognized as being there.

http://thesciencenetwork.org/media/v...Transcript.pdf

Side note to Rosie: I strongly recommend that you watch the full 1 hr. 12 min. interview. Llinás begins with a central thesis ”If our cells [acting as effectors] don’t feel, then we won’t,” before launching into this wonderful description of the fourth year of his life, spent upon invitation in the home of his widowed Columbian grandfather, a professor of psychiatry-neurology, which remembered “every millisecond of it. Really.” It was not for nothing that the introduction to the Colombian edition of I of the Vortex: From Neurons to Self (2002) was written by Gabriel Garcia Marquez! In fact, immediately after noting how lucky he was to have attended a high school where members if the faculty were among the leading European academics of their time – who had fled WWII – and who taught concepts instead of facts, he ticks off a number of salient points, how electrical stimulation removes dystonia and that “the mind is soluble in local anesthetic.”

Then too, the interview is just so filled with so much brilliant stuff I would be a bore in trying to repeat it. Viz., volition is what is already happening somewhere else in the brain and taking possession of it; “free will is knowing what you are going to do, that’s all. Not necessarily willing it.” (A point further developed in The 'prediction imperative' as the basis for self-awareness, Llinás RR, Roy S, Philos Trans R Soc Lond B Biol Sci. 2009 May 12; 364(1521):1301-7, FULL TEXT @ http://www.ncbi.nlm.nih.gov/pmc/arti...tb20080309.pdf) And, the more we learn about what we are, the more we will find others interesting and likeable. Trust me: there is amazing stuff in there.

The central thrust of “Abnormal thalamocortical activity in patients with Complex Regional Pain Syndrome (CRPS) Type I” http://www.rsds.org/2/library/articl..._Pain_2010.pdf is captured for our purpose in the “Discussion” at pp. 8 – 10 of the Epub. For anyone who is at all familiar with the current medical literature on CRPS, it is disappointing to realize how little if any of the EEG literature is apparently followed by those academic neuroscientists and neurologists specializing in either CRPS or NPP. A point made in the opening sentences to the accompanying Commentary, Thalamocortical dysrhythmia and chronic pain, Jones EG, Pain 2010 Jul; 150(1):4-5. Epub 2010 Apr 14:

The paper by Walton et al. [13] in this issue of Pain brings a new perspective to the problem of central pain, in this case complex regional pain syndrome without peripheral nerve injury (CRPSI). It is a perspective that may have escaped the notice of many pain scientists and sensory physiologists.

(See, e.g., Brief, low frequency stimulation of rat peripheral C-fibres evokes prolonged microglial-induced central sensitization in adults but not in neonates, Hathway GJ, Vega-Avelaira D, Moss A, Ingram R, Fitzgerald M, Pain 2009;110-118, FULL TEXT @ http://www.rsds.org/2/library/articl...J_Pain2009.pdf and Treatment of CRPS with ECT, Wolanin MW, Gulevski V, Schwartzman R, Pain Phys. 2007; 10:573-578, FULL TEXT @ http://www.rsds.org/2/library/articl...chwartzman.pdf) Check out the following excerpts from the Discussion section of “Abnormal thalamocortical activity in patients with Complex Regional Pain Syndrome (CRPS) Type I” and their associated footnotes, which among other things, make the heretofore “unknown mechanism” by which electrical stimulation alleviates chronic pain all too apparent:

Our finding of somatosensory activity corresponding to the reported region of spontaneous pain is consistent with such localization in evoked pain studies (see [71]). However, domination by low frequency activity (Figs. 3A and 4) suggests that these neurons do not participate directly in pain localization. Rather, these neurons induce increased activity in adjacent cortical regions through an edge effect [37,39]. A reduction in the normal lateral inhibition would force adjacent cortical areas into spontaneous and protracted high frequency oscillations resulting in a constantly present sensation. This interpretation is consistent with MEG [30,43] and EEG [60] studies of patients with unilateral CRPS I showing that the CNS signal evoked by sensory stimulation of the affected limb is greater than that evoked by simulation of the unaffected limb. Changes of S1 are also seen in other types of NPP [13,14,45,74]. Pain localization is provided by such somatosensory activation while the emotional component is provided by activity in limbic regions.

* * *

An attractive interpretation of these data is that CRPS I reflects a neurological ‘‘disconnection syndrome” resulting in a disturbance in thalamocortical interplay and a chronic dynamically recurrent TCD. Electrophysiologically, TCD is characterized by hyperpolarization of thalamic neurons, low frequency resonant recurrent interaction between thalamic and cortical neurons [35], and the presence of an edge effect. Thalamic neuronal hyperpolarization occurs by excess inhibition [34], disfacilitation from thalamic deafferentation [35,76], or block of excitatory ligand-gated channels [72]. Low frequency rhythmic MEG activity as seen here is, we propose, the result of a functional channelopathy. Thus, a chronic deinactivation of thalamic Cav3.1 channels [7,40] results in low frequency spontaneous thalamic rhythmicity. Indeed, low frequency thalamic bursts have been recorded from NPP patients [26].

* * *

Thalamic neuron hyperpolarization is consistent with the finding that somatosensory cortical neurons in CRPS I patients have a reduced sensitivity to tactile perception [58] and a reduced cortical representation of the affected body region when evoked by natural or electrical stimulation [30,43,58,60]. Thus, this reduction may result not only from an impoverished input but also from a reduced responsiveness of the remaining cells to the small natural inputs they might receive. There is an emerging theme of TCD in NPP. Low frequency oscillations and shift of the power spectra toward lower frequencies have consistently been found in other NPP states as recorded from cortex [6,10,69,70,73] and thalamus [20,25–27,33,69]. A study of patients with chronic, severe NPP reported a high temporal coherence between central lateral thalamic field potentials and cortical EEG oscillations at 4–9 Hz [68]. Such high thalamocortical coherence supports the role of the thalamus in synchronizing the cortical oscillations seen in animal studies [40]. An edge effect has been observed in other types of NPP as increased beta activity [28,69,73] and as increased gamma activity in tinnitus [9,39,63,77] and migraineurs [8]. This edge effect has been proposed to generate the positive symptoms in pain and allodynia [27,36,70], in movement [53,67], and in psychiatric disorders [36,38,39,77]. Thus, a common neuronal mechanism may underlie these disorders. TCD in various disorders is distinguished by the region of thalamic nucleus with low frequency oscillations [26]. The presence of high frequency activity is a subject of interest for future MEG studies of CRPS I.

* * *

Concerning stimulation, any stimulus resulting in thalamic neuron depolarization, and thus normal rhythmicity and responsiveness, will be beneficial in CRPS I patients. The effects of spinal cord and brain stimulation in phantom pain [62] probably result from thalamic depolarization by collateral afferent activity and possible sprouting-type plasticity. Also based on TCD circuitry, a therapeutic microlesion of the Field of Forel† may provide lasting pain relief in CRPS I as in other types of NPP [27,28]. Following campectomy‡, abnormal low and high frequency activity and reported pain level gradually decrease together [68,69].

† Fields of Forel is an area in a deep part of the brain known as the diencephalon. It is below the thalamus and consists of three defined, white matter areas of the subthalamus. These three regions are named "H fields" (for Haubenfelder). The first, field H1, is the thalamic fasciculus, a horizontal white matter tract between the subthalamus and the thalamus. These fibers are projections to the thalamus from the basal ganglia (globus pallidus) and the cerebellum. H1 is separated from H2 by the zona incerta. Field H2 is also made up of projections from the pallidum to the thalamus, but these course the subthalamic nucleus (dorsal). Field H3 (aka the prerubral field), is a large zone of mixed gray and white matter located just rostral (In front) of the red nucleus. http://en.wikipedia.org/wiki/Fields_of_forel

‡ Limited neocortical removal. Presurgical strategies and epilepsy surgery in children: comparison of literature and personal experiences, Munari C, Lo Russo G, Minotti L, et al, Childs Nerv Syst. 1999 Apr;15(4):149-57

Notes
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[38] Llinas RR, Choi S, Urbano FJ, Shin HS. Gamma-band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice. Proc Natl Acad Sci USA 2007; 104:17819–24 [see comment].

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[45] Maihofner C, Neundorfer B, Stefan H, Handwerker HO. Cortical processing of brush-evoked allodynia. Neuroreport 2003; 14:785–9.

[53] Moazami-Goudarzi M, Sarnthein J, Michels L, Moukhtieva R, Jeanmonod D. Enhanced frontal low and high frequency power and synchronization in the resting EEG of parkinsonian patients. Neuroimage 2008; 41:985–97.

[58] Pleger B, Ragert P, Schwenkreis P, Forster AF, Wilimzig C, Dinse H, Nicolas V, Maier C, Tegenthoff M. Patterns of cortical reorganization parallel impaired tactile discrimination and pain intensity in complex regional pain syndrome. Neuroimage 2006; 32:503–10.

[60] Pleger B, Tegenthoff M, Schwenkreis P, Janssen F, Ragert P, Dinse HR, Volker B, Zenz M, Maier C. Mean sustained pain levels are linked to hemispherical side-to-side differences of primary somatosensory cortex in the complex regional pain syndrome I. Exp Brain Res 2004;155:115–9.

[62] Ray N, Jenkinson N, Kringelbach M, Hansen P, Pereira E, Brittain J, Holland P, Holliday I, Owen S, Stein J, Aziz T. Abnormal thalamocortical dynamics may be altered by deep brain stimulation: using magnetoencephalography to study phantom limb pain. J Clin Neurosci 2009; 16:32–6.

[63] Richter GT, Mennemeier M, Bartel T, Chelette KC, Kimbrell T, Triggs W, Dornhoffer JL. Repetitive transcranial magnetic stimulation for tinnitus: a case study. Laryngoscope 2006; 116:1867–72.

[67] Sarnthein J, Jeanmonod D. High thalamocortical theta coherence in patients with Parkinson’s disease. J Neurosci 2007; 27:124–31.

[68] Sarnthein J, Jeanmonod D. High thalamocortical theta coherence in patients with neurogenic pain. Neuroimage 2008; 39:1910–7.

[69] Sarnthein J, Stern J, Aufenberg C, Rousson V, Jeanmonod D. Increased EEG power and slowed dominant frequency in patients with neurogenic pain. Brain 2006; 129:55–64.

[70] Schulman JJ, Zonenshayn M, Ramirez RR, Ribary U, Llinas R. Thalamocortical dysrhythmia syndrome: MEG imaging of neuropathic pain. Thalamus Relat Syst 2005; 3:33–9.

[71] Schwenkreis P, Maler C, Tegenthoff M. Functional imaging of central nervous system involvement in complex regional pain syndrome. Am J Neuroradiol 2009:1–6.

[72] Serulle U, Urbano F, Lisman J, Llinas R. Increase of oscillatory inhibitory synaptic events in thalamic relay neurons after inhibition of NMDA-mediated transmission. Washington, DC: Soc Neurosci; 2008.

[74] Tecchio F, Padua L, Aprile I, Rossini PM. Carpal tunnel syndrome modifies sensory hand cortical somatotopy: a MEG study. Hum Brain Mapp 2002;17:28–36.

[76] Wang G, Thompson SM. Maladaptive homeostatic plasticity in a rodent model of central pain syndrome: thalamic hyperexcitability after spinothalamic tract lesions. J Neurosci 2008; 28:11959–69.

[77] Weisz N, Moratti S, Meinzer M, Dohrmann K, Elbert T. Tinnitus perception and distress is related to abnormal spontaneous brain activity as measured by magnetoencephalography. PLoS Med 2005; 2:546–53.

If anyone wants to acknowledge some frustration that two sides of the same “Dept. of Neurology brain” have not been communicating for the last two decades or so, this may be the time to do so.

Mike