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Showing entries tagged cortical development.  Show all entries

December 4, 2011

Phantom Limb Pain and Cortex Reorganization


Feeling pain in the arm that you lost in an accident? Does your arm you lost in the war itch terribly? This sensation of feeling like a lost limb is still attached to the body is known as a phantom limb pain (PLP). The purpose of this study was to identify plastic changes in the somatosensory and motor cortex in patients with and without phantom limb pain. Most sensations regarding these phantom limbs are painful as if the limb was contorted into an awkward position. Although in many cases the complaint is pain, some patients experiencing a phantom limb experience sensations such as itching, burning, or feeling as though the limb is too short. Although PLP is more common in the early stages following an amputation, some have reported pain for years after. It was previously discovered that PLP had a strong correlation with representational plasticity in the somatosensory cortex; however, its correlation with the plasticity in the motor cortex was unknown. This experiment used methods such as Transcranial Magnetic Stimulation (TMS) of the motor cortex, and neuroelectric source imaging of the somatosensory cortex to study the correlation of plasticity in these cortices.

In this study, participants included five upper-limp amputees experiencing PLP and five upper-limb amputees experiencing no PLP. A German version of the West Haven- Yale Multidimensional Pain Inventory was used to evaluate each patient's stump and limb pain. To test for motor reorganization, focal TMS was delivered from a magnetic stimulator through an 8-shaped magnetic coil. The leads were positioned to cause currents to flow approximately perpendicular to the central sulcus, optimally causing the largest peak-to-peak motor evoked potential in each muscle. In patients experiencing PLP, a map of outputs determined by neuroelectric source imaging of EEGs done showed significantly larger motor-evoked outputs on the side lacking the arm than the side with the remaining arm, whereas excitability in the motor neurons of amputees remained unchanged. Since it was previously known that motor reorganization in amputees takes place at a cortical level, the leap was made that. "It is likely that cortical mechanisms are also responsible for the differences in reorganization observed in both patient groups (Karl, Anke et. al., 2011)."

While these findings support the notion that increased plasticity is present in the motor cortex of PLP patients, the evidence used to support this main point is presented in a very odd fashion. Immediately following this claim about cortical mechanisms and presenting supporting evidence, they state that their results "do not rule out the possibility of additional subcortical reorganization." This statement is saying that other factors could be causing or contributing to the claims being made by their research, thus making the research inconclusive as a whole. Another problem with the research methods is that the patient's amputations all occurred at different times. Some more recent than others, which could have a profound effect on the plasticity levels reached at the time of testing.
All in all the research conducted further supports already claimed notions, while having no real additions of any validity or originality. These limitations could be reduced by choosing patients who's amputations occurred within the same month. The potential that could be reached through studies similar to this are immense, but further research needs to be conducted in order to draw on more valuable conclusions.




The Journal of Neuroscience, 15 May 2001, 21(10): 3609-3618;
Posted by      Madelyn K. at 8:29 PM MST

October 22, 2011

Sleep and spines modulate your mind...and your brain?


"The mind is the brain doing its job." - Simon LeVay, 1994

We know that sleep is good for us: it's a daily, regularly- or irregularly-scheduled body and brain maintenance check. The sleep/wake cycle maintenance staff in particular is profoundly important in synaptic renormalization (homeostasis) by modulating (decreasing) synaptic size and/or strength in the adult brain. In the adult brain; surprisingly, this doesn't exactly hold for the adolescent brain, where sleep/wake cycle maintenance staff is responsible for more synaptogenesis (synaptic formation) and synaptic pruning (synaptic elimination).


A recent article published in Nature Neuroscience examined the process of cortical development (that involves synaptogenesis and pruning) in adolescent YFP-mice (through two-photon microscopy) as a function of different sleep/wake cycles: W1S2 mice (wake followed by sleep), and S1W2 mice (sleep first followed by wake). Mice were allowed to sleep or kept awake for each behavioral state (sleep/wake) for durations that mimic physiological sleep/wake cycles (6-8 h) and then imaged. Interestingly enough, they found overall decreased spine density in W1S2 mice and increased spine density in S1W2 mice; there was no variation observed in mice in early or late adolescence. Waking results in a net increase in cortical spines, and sleep is associated with net spine loss.
A third experimental group of W1SD2 mice (wake followed by sleep deprivation), to control for decreased spine density as a function of the passage of time showed a net increase in synaptic density.


In summary:
Wake followed by sleep (W1S2) = spine loss
Sleep followed by wake (S1W2) = spine gain
Wake followed by sleep deprivation (W1SD2) = spine gain

Sleep might actually be bad! (...for dendritic spines, that is)


The wake-sleep deprived group presents an interesting case. Sleep-deprivation, akin to pulling an all-nighter, shows a net increase in spine density. Therefore, sleep deprivation is one way to keep your dendritic spine density (that is, until you crash of exhaustion). Sleeping for the recommended 8 hours a night is also a default option. For those of us in adolescence, retaining spine density though sleep-deprivation is still theoretically a viable option. A different experiment conducted by the same researchers imaged the mice after 2-3 hours of sleep (short sleep) or wake (short wake). Both groups showed no net changes after short sleep or short waking. It may be theoretically possible to maintain spine density through a sleep-deprivation following wake with short sleep sleep/wake cycle (power naps anyone?).


This article concludes by suggesting that behavioral state modulates spine turnover in a manner consistent with the need for synaptic homeostasis; in the adult brain this translates into synaptic renormalization, and in the adolescent brain (regardless of exact developmental stage of adolescence) this translates into synaptogenesis and synaptic pruning. Sleep may therefore facilitate spine elimination or spine loss in certain phases of development. Sleep deprivation during adolescence may affect synaptic turnover, as it blocks sleep-related spine pruning; however, it does not result in a further increase in spine density. It is currently unclear to what extent the role of sleep in spine elimination is permissive and/or instructive.


So what does sleep and spine density have to do with anything? In the adult brain, it decreases synaptic size and/or strength; in the adolescent brain, it modulates synaptic pruning during a period of massive synaptic remodeling. Synaptic spine density is a part of how the brain does its job. Spine density therefore affects the mind (the brain doing its job that feeds to the mind). Changes in our minds are therefore a result of the brain doing its job differently, and how the brain does its job differently can involve changes in synaptic spine density. Spine density subsequently affects the different jobs of the brain; spine density affects the mind. Sleep (the sleep/wake cycle), therefore, is especially critical in cortical development during adolescence in modulating synaptic spine density (long-term potentiation anyone?)

I should probably get more sleep myself...

Source: http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.2934.html
Posted by      Patricia W. at 10:19 PM MDT
displaying most recent comments (1 ommitted) | Comments (4)
  Patricia Wuu  says:
This particular study focused on the adolescent brain so yes to your first question. In the adult brain the synapse strength is the only thing that changes (the paper mentions size). In terms of the sleep deprivation, what they explicitly give is 6-7 hours of sleep deprivation during the day; also included though is sleep deprivation after waking at night, where they don't specify the exact time. For the last question, though they don't address this, I think studying that in a mouse and then translating that to a human would be challenging, but maybe someday these researchers might decide to look into it!
Posted on Thu, 27 Oct 2011 7:49 PM MDT by Patricia W.
  Christina Uhlir  says:
Patricia,

Thanks for responding to my question in such depth. I, too, hope that there will be more studies that actually link our sleep needs to those of the mice as well, it would be interesting to finally learn how we can improve our sleep habits to maximize our cognitive abilities.
Posted on Thu, 27 Oct 2011 8:55 PM MDT by Christina U.
  play game  says:
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Posted on Mon, 28 Jan 2019 12:06 AM MST by play g.




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