by Heidi Norman
Next I begin Doidge’s book. It is a revelation; it gives me hope that I can do something about my malfunctioning brain.
At the time of my postgraduate clinical training, it was accepted that we had a finite number of neurons, with largely fixed connections. There was little a brain-injured person could do for cognitive rehabilitation. It was understood that brain function improved spontaneously over the first six to 12 months, and thereafter it plateaued. It wasn’t clear why this pattern occurred. The brain-injured person was a passenger in their rehabilitation, not the driver. The more diffuse the brain injury (strokes often cause diffuse injury), the more wide-ranging the resulting deficits, and the slower the recovery.
Doidge tells me the brain is plastic: new connections can be made between existing neurons, and sometimes new neurons can grow. Neuroplasticity happens by focusing the mind’s attention in specific ways so neurons that ‘fire together, wire together’. Like technicians, we can change our brain’s circuitry to suit our purposes. He mentions research by Alvaro Pascual-Leone, who, using transcranial magnetic stimulation, demonstrated that blind people who learned to read the raised dots in braille developed larger ‘maps’ in the motor cortex for the fingers used for ‘reading’ than for their non-reading fingers. The area devoted to these fingers in their motor cortex was also larger than the equivalent area in those who couldn’t read braille. In the blind person, the occipital area of the brain, which is usually devoted to vision, gets taken over by other functions, such as sound.
I already have some understanding of brain neurology through my clinical training. But Doidge is telling me that I can apply this knowledge to myself. I’m surprised by how uplifted I feel as I absorb his ideas; it takes me out of my life’s messiness. I want to know more.
Each neuron has a bulbous cell body with dendrites, like spidery arms, sprouting off it. The rest of the neuron is made up of a long, thin fibre – the axon – that ends in numerous fist-shaped synapses. The dendrites and axon of a neuron can grow ‘sprouts’ to make new connections. A connection between neurons is most often made when the synapse of one comes into proximity to the dendrite of another. Information passes along the axon via an electrical impulse until it reaches the synapse. Here, neurotransmitters – the brain’s chemical messengers – are released, and they move, in microseconds, through the minute gap between the synapse and the neuron it is cosying up to. As a newly made connection is reactivated over and over, the synapse and dendrite become sensitised to each other: they communicate more efficiently, like good friends.
A single neuron can connect to thousands of other neurons, and it is this capacity for neuronal connectedness that provides the landscape for neuroplasticity. I think of it as akin to families. A small nuclear family has few members to draw on for knowledge, skills, and resources. If something happens to one or two of its members, the family unit is in jeopardy. The advantage for the nuclear family is that communication between them is quick. Yet an extended family, with multiple generations, draws on more resources. As long as they cooperate, this family has greater resilience and capability because of their wide-ranging connectedness.
The neurotransmitters in the brain – especially glutamate and gamma-aminobutyric acid (GABA) – act like neuronal ‘on’ and ‘off ’ switches. Glutamate is excitatory, activating neurons, and GABA is inhibitory, reducing activity. This ‘on’ and ‘off ’ process is the stepping-stone of neuroplastic change.
There are also many other neurotransmitters that modulate neuronal activity. Focusing attention on something activates the nucleus basalis (above the brain stem) to release acetylcholine, which diffuses throughout the brain, helping to sustain this attention. Dopamine is released when a reward is expected or a goal has been achieved. Noradrenaline is released when we come across something new, alerting our brain to take notice. Serotonin is active in creating the emotional quality of wellbeing. So the acts of focusing attention and experiencing novelty, reward, and emotional tone all help to cement neuroplastic changes.
When a number of neurons fire together, they become a neural network, threading its way throughout the brain. A particular memory is distributed through the brain as a living chemical and electrical trace, and the more neurons employed in the memory, the more secure it is. Recall of a memory reactivates the same neural network that responded to the original event; remembering requires the brain to pull together the sensory, motor, cognitive, and emotional components of the memory. The hippocampi act as the managers in coordinating this recall. The damage to my left hippocampus and temporal lobe probably explains my difficulty in recalling the names of things and people, and in remembering what others tell me. The recall of a complete memory is like a successfully baked cake. A cake requires flour, baking powder, eggs, butter, sugar, and flavouring, but if one of these ingredients is missing, the cake will still be cake-like, just not as complete. Similarly, when memory recall is altered by brain damage, there is still a memory, although it will be missing elements of the full memory.
Certain brain chemicals cement neuroplastic change by their actions on synapses and neurons. Brain-derived neurotropic factor (BDNF) is a protein that helps to maintain existing neurons and encourages the growth of new neurons and synapses; its supply in the brain is key to neuroplasticity. In the family analogy, BDNF is like the food the family members eat; the amount and quality of this food is critical to their wellbeing. Most neurons have a myelin sheath surrounding the axon. As the neuron becomes more active, the myelin sheath grows in thickness. This increases the speed at which an electrical impulse travels along the axon. BDNF facilitates myelinisation.
Neuroplasticity not only means new connections between existing neurons. In a few parts of the brain, new neurons grow from stem cells, in a process called neurogenesis. This is the part that really excites me, because neurogenesis has been found to occur in the hippocampus. Can I restore my damaged left hippocampus and get my memory working again?
I best understand the variations of neuroplasticity using a road analogy: new sections of road can be built to provide ways around blockages in the existing road network (synaptogenesis), existing roads can be made easier to travel by widening and resurfacing (myelinisation), and completely new roads can be built (neurogenesis). The type of change governs the time required: synaptogenesis takes minutes to hours; neurogenesis takes weeks; and myelinisation takes months. Quick neuroplastic changes strengthen existing neural connections, while the slower, but longer lasting, changes rely on the formation of new connections and new neurons.
My experience of how hard it is to maintain a conversation and how noxious certain sounds have become – some people’s voices, music in shopping centres – points me to the belief that I have an auditory-processing problem. Dr Small has told me that the damage to my brain, while most obvious in the occipital lobe, has also encroached into the temporal lobe on the left side, an area critical for understanding speech. This could explain why I forget what others tell me, and my difficulty in keeping up in conversation: if I’m slow at taking in what people say, there’s less chance of remembering what’s been said.
I can hear speech, and I can make the sounds of the words in speech. But my brain finds it difficult to translate the sounds of speech into engrams – neural representations of words. And there’s my difficulty with finding the right word.
According to Doidge, this can be due to ‘fuzzy engrams’. It reminds me of my trip to Paris in my early twenties, when I relied on my schoolboy French. I could pick up a word or phrase when listening to the native speakers, feeling as if I should be able to understand them, but I couldn’t, really. If my neural circuits for making others’ speech intelligible were once dual-lane freeways, they are now single-lane highways; my brain is trying to handle the same amount of auditory traffic, but with reduced neural infrastructure. No wonder I’m drawn to quiet places, soft voices, and people who speak slowly.
I begin to wonder: could I retrain my brain specifically to improve au
ditory processing? Doidge mentions Posit Science, a provider of training programs aimed at reducing cognitive decline in the elderly, and I decide to investigate further.
When I look at the Posit Science website, it says that they offer two programs designed to help the elderly with the cognitive decline associated with ageing. The InSight program improves visual processing. The Brain Fitness program improves auditory processing: forgetting names, slowness of thinking, difficulty in word retrieval, difficulty in deciphering speech, and fatigue in conversation. I’m not elderly, but this describes me perfectly. Could it work for me too?
* * * * *
When my Brain Fitness program turns up in the mail, I’m eager to get started.
For optimum results, Posit Science recommends 40 hours over eight weeks – five days a week, one hour per session. On the first day, I only manage 30 minutes; after this, rubber brain threatens to overtake me. The next day is the same, as is the following. This shows that I’m working to my limit. At this rate, it’s going to take me six months or more to complete it.
The program concentrates on building the basic auditory skills (pitch and phonemes), and then the components of speech (syllables and sentences), and finally comprehension (narratives). It contains six exercises. ‘High or Low’ trains for pitch in speech using frequency sweeps: a computer-generated sound begins low and rises in pitch, or begins high and lowers. It’s a sound like a zipper being opened or closed quickly. I listen to pairs of sweeps in my headphones. I have to decide if each sweep in a pair has gone upward or downward, and click on the correct sequence of up and down arrows on the screen. The program picks up my progress, making the sweeps quicker and reducing the time gap between them. The brain needs to be pushed to improve.
The second exercise, ‘Tell Us Apart’, uses phonemes – the individual sounds that make up words. In the word ‘dog’, for example, there are d, o, and g sounds. The program presents similar-sounding phonemes: for example, the sounds ‘dah’ and ‘gah’. The sounds are hard to tell apart. I perform very badly.
‘Match It’ is like the card game Memory. A matrix of cards is presented facedown on the screen. Each card has a syllable associated with it, and within the matrix there are pairs of syllables. Some of the syllables are dissimilar in sound: for example, ‘baa’, ‘fo’, and ‘pu’. Other syllables sound similar: for example, ‘sho’, ‘stu’, and ‘sa’. I am allowed to click on two cards and hear the sounds being spoken. I work my way through the matrix. This is training my working memory for spoken words. The matrices increase from eight to 16 to 24 to 30 cards.
I excel at ‘Match It’, compared with the other exercises; it’s encouraging to still be good at something. Perhaps it shows that when I can use my visual memory, it aids my overall memory. As I progress onto the larger matrices, I notice that I can let go of mentally rehearsing the sequence of sounds I’ve just heard. Instead, when I click on a new card to hear a sound I’ve heard before, I let my mouse drift over to the card that ‘feels’ like the match and click on this. Most often, it is correct. Somehow, my subconscious processing has become faster and more accurate.
I’d love to spend more time doing ‘Match It’, but the Brain Fitness program, like a good teacher, soon learns my weak areas and focuses on the exercises that most challenge me. One of these is ‘Sound Replay’. It presents syllables such as ‘baa’, ‘fo’, and ‘laa’ as a memory-span exercise, asking me to remember a series of such sounds. The voice names a random sequence of syllables, starting with two and then moving to three, four, five, and more. I need to indicate which syllables were said, and in what order. This is training my capacity to discriminate sounds and is building my auditory working memory. I do poorly on this exercise – the sounds quickly enter the fog.
In ‘Listen and Do’, I am presented with a scene that contains people, animals, objects, and buildings. I hear a set of instructions: a sequence of things that I am to click on. Once the instructions are given, I need to click on the objects in the same order. As the exercise advances, I have to move a person or an animal to a new location. I’m okay with this exercise, once I develop a strategy for it. I draw imaginary lines between each named object, giving me a visual shape to remember. This resembles my real-life task of visualising a mental list of things to do and staying on track until they are all completed.
The final exercise, ‘Storyteller’, is the most enjoyable. The voice tells a story of everyday events and interactions between people. At its completion, I need to answer ten, 15, or 20 multiple-choice questions about the story. There are five stories in all, and they become progressively more complex. This is training short-term memory and comprehension – being able to remember and understand details in conversation.
Progress bars appear on the screen during each exercise, and I strain to get to the next level of difficulty. There’s a sense of achievement (a dopamine hit) when I reach a new level, and the program rewards me with animated fireworks and music. At the end of every session I can access a summary page, which lets me know how I’m going. This is reassuring, even though it shows how poorly I’m performing in most exercises: it gives me a baseline from which I can see increments of improvement.
As I get into the rhythm of training, most days I advance on an exercise or stay at the same level. But sometimes I have an off day. That’s when I see, in the form of the progress bar, how dramatically my performance drops when I’m mentally or physically fatigued – a clear indication that fatigue really does affect my capacity to function.
After one month of doing 30 minutes most days, I have progressed to some degree in all exercises. I haven’t noticed a great difference in my auditory processing in the real world, so I’m a little discouraged. But the cheerful male voice that explains what each exercise does and why it is useful shows a picture of the brain with coloured lines connecting the areas that each exercise works on, reassuring me that I am making new neural connections. If it doesn’t work, I’ve only wasted some time and dollars.
I’m consistent with the Brain Fitness training, even when I’m feeling off. At first I do the session mid-afternoon, before I get rubber brain for the day. But then I realise that I make better progress in the morning. I change tack, training just before lunch.
By the six-week mark, I’ve noticed a real difference. My progress has been gradual, but all of a sudden the world is easier to comprehend, as if a door has opened. Other people’s speech seems clearer; everyday social conversation is simpler. I still lose track in longer, more involved conversations, but I’m confident now that I’m showing improvement. My brain is coming back online and is starting to work with me.
* * * * *
Fifteen months post-stroke, and my auditory processing has improved dramatically – in particular, my comprehension of speech and my working memory. I can think again, hold conversations, and make sense of what I hear and read.
In a medical sense, I have not completely recovered, neurologically or psychologically. When is a disability a disability? I conclude that in the case of a hidden impediment, such as brain injury, it is only viewed as a disability when others recognise the deficits. And it doesn’t help that it has taken me 15 months to work out what has changed since the stroke: it is often only in new situations that I learn what I can do and what I cannot. It’s a meandering way to find out my limits, but there is no medical test that will work this out for me; life is the only test.
However, I feel recovered, in an important way. I have strengths that I didn’t have prior to the stroke, and I have accepted that some of the old strengths, such as the sharp memory, are gone. I’m not back to where I was yet, but I’m steadily improving. And in other ways, I’m far ahead of where I was. I’ve rescued my brain.
It’s all in your mind: The feeling of ‘wetness’ is an illusion
Why aren’t we dead yet?
The mind of Michio Kaku
Small mammals vanish in northern Australia
Dyani Lewis
Just a
fter dawn, Danielle Stokeld sets out on foot to inspect small mammal traps nestled among spindly eucalyptuses and pandanus pines in Kakadu National Park in Australia’s far north. In spite of knee-high spear grass, the ecologist with the Northern Territory’s Department of Land Resource Management zips through her 2.4 kilometre route, managing to check all 117 traps in less than an hour. The reason for her alacrity: every last trap is empty.
Back at Kakadu’s South Alligator ranger station later on that cool July morning, other researchers say they have fared no better. After two weeks of trapping, the dire reality is becoming clear. From 4000 traps at six sites, all the researchers were able to snare were a single delicate mouse and two northern quolls – spotted hedgehog-sized marsupials with long, fleshy tails.
In northern Australia, mammal populations are in free fall. Over the past two decades, scientists have documented sharp declines in quolls, bandicoots, and other native fauna. The plight of these animals has grown so desperate that in July 2014, the Australian government appointed the nation’s first threatened species commissioner, Gregory Andrews, a Department of the Environment staffer now tasked with devising broad approaches to stem the tide of extinctions. The solutions are not obvious, but mounting evidence points to the arch villain: feral cats, aided and abetted by fire.
The European influx beginning two centuries ago turned the island continent into a crucible of extinction. Since then, 29 land animal species have gone extinct, including, most famously, the thylacine, or Tasmanian tiger, which winked out early last century. Other vanished fauna include species of bettongs, bandicoots, potoroos, bilbies, and wallabies. Australia’s losses represent about a third of the world’s mammal extinctions over the past 500 years. Many disappeared before 1950, after getting squeezed out of habitats and falling prey to invaders including cats and European red foxes. Another invader, the cane toad, has been a bane to northern quolls, which eat the toads and succumb to poison they secrete.
