Archive for December, 2013

The Nativity – by G. K. Chesterton

Tuesday, December 24th, 2013

The thatch on the roof was as golden,
Though dusty the straw was and old,
The wind had a peal as of trumpets,
Though blowing and barren and cold,
The mother’s hair was a glory
Though loosened and torn,
For under the eaves in the gloaming
A child was born.

Have a myriad children been quickened,
Have a myriad children grown old,
Grown gross and unloved and embittered,
Grown cunning and savage and cold?
God abides in a terrible patience,
Unangered, unworn,
And again for the child that was squandered
A child is born.

What know we of aeons behind us,
Dim dynasties lost long ago,
Huge empires, like dreams unremembered,
Huge cities for ages laid low?
This at least–that with blight and with blessing
With flower and with thorn,
Love was there, and his cry was among them,
“A child is born.”

Though the darkness be noisy with systems,
Dark fancies that fret and disprove,
Still the plumes stir around us, above us
The wings of the shadow of love:
Oh! princes and priests, have ye seen it
Grow pale through your scorn?
Huge dawns sleep before us, deep changes,
A child is born.

And the rafters of toil still are gilded
With the dawn of the star of the heart,
And the wise men draw near in the twilight,
Who are weary of learning and art,
And the face of the tyrant is darkened.
His spirit is torn,
For a new King is enthroned; yea, the sternest,
A child is born.

And the mother still joys for the whispered
First stir of unspeakable things,
Still feels that high moment unfurling
Red glory of Gabriel’s wings.
Still the babe of an hour is a master
Whom angels adorn,
Emmanuel, prophet, anointed,
A child is born.

And thou, that art still in thy cradle,
The sun being crown for thy brow,
Make answer, our flesh, make an answer,
Say, whence art thou come–who art thou?
Art thou come back on earth for our teaching
To train or to warn–?
Hush–how may we know?–knowing only
A child is born.

Merry Christmas, everybody!

Ground zero for Alzheimer’s Disease?

Monday, December 23rd, 2013

A new study in the journal Nature Neuroscience involved very high-resolution functional imaging on the brains of older mice, and humans, who exhibited early signs of Alzheimer’s Disease. They traced the earliest signs of dysfunction to a small  and well-defined structure in the temporal lobe called the lateral entorhinal cortex. (Entorhinal, if you must know, literally means “in the nose”. Sniff. But it’s not really in your nose, so don’t worry, you can blow your nose with confidence.) The entorhinal cortex is one of a set of structures located deep toward the middle of the temporal lobe that are critical for storing new memories, which makes sense, given that one of the primary features of dementia is the inability to remember things.

Anyway, the thing I found particularly fascinating about this study is that it also found that the disease progressed to other structures, elsewhere in the brain, to which the lateral entorhinal cortex sends its signals. The authors surmise that the transfer of the disease is not through some structural or anatomical mechanism, such as the movement of toxic stuff down the fibres between the entorhinal cortex and the other sites. Instead, they believe that the deterioration of the downstream structures is caused functionally: that it happens because these sites end up being under-activated by the compromised entorhinal cortex. This could have implications for functional treatments aimed at altering brain activity patterns, because there’s a possibility that if we can keep those downstream structures active by spurring them into action somehow – such as by neurofeedback or brain stimulation – then we could potentially slow or halt the progression of the disease. Who knows, even functional activation of the entorhinal cortex itself may have some benefit.

Dementias such as Alzheimer’s disease are incredibly important at this moment for Western societies, because we are heading into a period during which we will have huge numbers of elderly citizens, many of whom will have dementing disorders. These disorders are going to create a huge strain on society’s resources, because they’re associated with a need for high levels of care and supervision, so anything that can potentially reduce this disease burden is definitely worth paying attention to.

Here comes neurofeedback!

Wednesday, December 18th, 2013

Just looked at this figure from a new issue of the journal Biological Psychology. The current issue is dedicated completely to scientific papers on neurofeedback. The editor of the special issue, Dr. John Gruzelier, uses this figure to show how much research interest has increased in neurofeedback over recent years. This graph shows how many academic papers on the topic can be found, plotted according to the year of publication:

Neurofeedback has been around for about fifty years, but it’s only recently begun really to catch the attention of the scholarly community. The acceleration in scientific interest in the subject reflects growing recognition that neurofeedback works, and growing interest in studying how it works, and what sorts of things it works for. Strap yourselves in, there’s exciting times ahead!

Okay, so, what if stimulant meds actually don’t work over the long term?

Sunday, December 15th, 2013

The jury’s still out, but it’s beginning to look that way (see my recent post). That leaves a lot of people without recourse to any effective way to address the very real problems associated with ADHD, and many other conditions that have a component of reduced capacity for attention and self-control. The medical profession has nothing other than stimulant medications, and a couple of other drugs, to offer for attention disorders. As we’ve seen, although these medications work well in the short term, they aren’t effective in the long term, and may indeed make things worse rather than better. Psychotherapy and behavior therapy aren’t really helpful either, at least not in addressing the core neurological problem with self-control that underlies the various manifestations of the disorder.

This is where I believe neurofeedback offers a critical alternative, and really stands alone as a method of improving brain function among those who struggle with attentional control. Neurofeedback is a method of training the brain by giving it direct, real-time information on what it’s doing, and encouraging it to shape its activity in a desired direction. It’s done by recording the EEG (electroencephalogram), processing the EEG signal in real time, and translating one or more chosen qualities of the EEG into a form of auditory and/or visual feedback, such as an animation on a computer screen, or music whose volume or pitch changes as the chosen EEG variable rises and falls.

Neurofeedback is essentially a variation on the learning theory principle of operant conditioning. That’s fancy psychologist-speak for the commonsense technique of rewarding a behaviour that one wants to see increase, and/or withholding the reward when that behaviour is absent. Anyone who’s ever trained a dog (or a kid!) knows how it works.

The innovation of  neurofeedback is that it treats the EEG as a “behaviour”  — which it is, really, when you think about it; it just doesn’t involve movement of the muscles that we normally associate with overtly visible behaviour. (Sorry, Americans, for the weird spelling of “behaviour”. We Canadians are a quirky lot.) There are other things we can’t see that are also behaviour — thinking a thought, for example. Anyway, neurofeedback rewards the brain for producing EEG waves that have certain chosen qualities, and lack other qualities that are undesired. The feedback is the reward, and, as with other forms of learning, repeated practice solidifies the newly learned behaviour until it becomes automatic and the brain just does it, without the need for further reward.

Neurofeedback differs from drug treatment in an important way, and that is that it uses the brain’s own innate change mechanisms, rather than imposing the change from the outside, as it were. This prevents the brain from treating the change as some new feature of the environment to be adjusted to, as is the case for the mechanism that leads to drug tolerance, described in my last post. Essentially, the brain doesn’t try and make adjustments to restore itself to “normal”; instead it redefines what’s “normal” and establishes a different standard for itself. That’s also why neurofeedback-induced changes hold over the long term, making it a permanent solution where medications are only temporary.

Whatsamatter with Ritalin?

Sunday, December 8th, 2013

Well, it’s complicated. It’s been known for a long time that it’s effective, almost scary-effective, for increasing attentional focus and decreasing restlessness and impulsivity, not just for those with ADHD, but for pretty much anyone who takes it. That’s why it’s become a favourite of university and professional school students looking for an edge in their studies. Its drawbacks in terms of side effects have also been known for a long time, and generally considered to be tolerable, if not desirable: the main risks are reduced appetite, weight loss, (among children) stunted growth, insomnia, and – for some – irritability or anxiety.

Ritalin is a stimulant medication, as are the other major “ADHD drugs” out there, including other variants on Ritalin’s basic molecule — methylphenidate — and amphetamine-based stimulants. All of these drugs work by increasing the availability of dopamine or similar chemicals in the communicating space between one neuron and the other, called the synapse. Basically, when one neuron “fires” (don’t you like the gun imagery? Bang!) it releases a neurotransmitter chemical (e.g., dopamine) into the space between it and the next neuron down the line, which has receptors to which the chemical binds, influencing the likelihood that it will itself “fire”, and so on. After spitting out the chemical, the upstream neuron very nicely tidies up the synapse by re-importing the leftover chemical and reusing it. Comforting to know my brain is better at keeping its workspace neat than I am. The way Ritalin and its cousins work is by interfering with this cleanup process, which leaves more dopamine sitting around in the synapse, increasing the likelihood of it binding onto the downstream neuron.

Anyway, thank you allowing me that little digression. The complicating factor is that the brain is an exquisitely adaptive organ. It’s always, always making adjustments based on its recent experiences and on what it’s recently been asked to do, or to stop doing. This property of brains is what gives animals, and especially humans, their amazing ability to learn and adjust to changes in their surroundings. The problem is that if brains never stop adapting, they’ll adapt to things that you may not necessarily want them to adapt to — like medications.

Here’s the rub: scientists have been increasingly raising questions about stimulants’ ability to continue to be effective over the long term, once the brain has had a chance to adjust to their presence. The more time goes by, the more doubt there is about their long-term efficacy. Several large-scale studies have found that, over periods of one to three years, people who take stimulants end up no better off than people who don’t, despite the fact that they showed dramatic improvements when they first took the drug. And now studies such as this one recently published in the journal PLOS ONE are starting to explain why. Essentially, what they’re finding is that, when the brain finds its synaptic cleanup ability degraded by the drug, it gradually responds by “up-regulating” (increasing) that same ability, which ends up leaving about the same amount of neurotransmitter in the gap as there was before. Unfortunately, what this means clinically is that symptoms tend to go back to where they were before, too.

But here’s perhaps the really pernicious part: what happens if the drug suddenly goes missing from the equation? Well, the cleanup crew is now staffed by a highly motivated, highly efficient team of crack cleanup commandos, so with the drug gone, it ends up creating a shortage of neurotransmitter in the synapse. Not enough dopamine. Effect? Even worse symptoms than you would ever have seen otherwise.

Now, imagine the effect this phenomenon would have on patterns of medication use. Parents of an ADHD kid saw remarkable changes for the better in their kid soon after he started Ritalin. That turned them into true believers: man, this stuff really works. Since then things haven’t been quite so amazing, but, you know, Junior’s growing, his body is changing, and he probably had some old habits that he still needs to outgrow. Plus, holy smokes, you should see the little guy when he misses a dose! He’s like a human typhoon, for gosh sakes! If we had any creeping doubts that the medication was doing something, that sure clears them away, and good golly, we do not wanna go back there again!

All of this might sound a little familiar: it’s a description of tolerance, which is exactly the same process by which people become addicted to stimulants such as caffeine, nicotine, methamphetamine and cocaine, as well as to other drugs such as alcohol and heroin. In every case the brain adjusts to the chemical’s presence so that greater doses are required to get the same effect, and withdrawal of the chemical leads to a dramatic physical and psychological crisis known as the drug’s withdrawal syndrome. In the end the only remaining reason for taking the drug isn’t to bring about some positive effect, it’s to maintain the status quo and prevent a decidedly negative effect.

More studies need to be done, obviously, but it’s looking like the sheen might be starting to come off the stimulant revolution. If it leaves people no better off than they would have been without taking it in the first place, and then enslaves them to a tolerance-and-withdrawal cycle, its merits are dubious at best.