Neuroplasticity is in.
Now there’s no doubt that the brain is plastic, able to rewire itself in response to damage or training, and that it’s more so than was generally believed, say, 20 years ago. It’s clearly an important and interesting field, but a little caution is warranted. Neuroplasticity can’t fix everything.
If the brain were infinitely plastic, brain damage would be no big deal. You’d get over it pretty quickly, so long as some of your brain was intact and able to rewire itself to compensate. Unfortunately, that’s rarely what happens. Well, unfortunately unless you’re a neurologist; they’d be out of a job if it were otherwise…
Swiss neurologists Bindschaedler et al have provided a nice example of the limits of neuroplasticity in a new paper: Growing up with bilateral hippocampal atrophy: From childhood to teenage.
Patient “VJ” was diagnosed with bilateral atrophy of the hippocampus at age 8. The damage almost certainly dated back a few hours after his birth which followed a normal pregnancy and delivery:
VJ had convulsions, then an episode of apnoea, which required treatment by phenobarbital and mask-assisted ventilation respectively. Hypertonia and hyperreactivity were followed by a period of hypotonia and somnolence during the 8 following days.
He seemed to make a full recovery, and never suffered another seizure. However, as he grew up, his parents noticed that he was forgetful and had difficulty concentrating. At the age of 8, he was referred for an MRI scan, which revealed severe atrophy of the hippocampus, and the related structures the fornix and the mammilary bodies, on both sides of the brain.
The diagnosis was hypoxic-ischaemic encephalopathy: a lack of oxygen. For some reason, the hippocampus is especially vulnerable to this; selective hippocampal damage is also common after carbon monoxide poisoning.
VJ is a bit like a childhood version of the famous adult patient HM, however, there are important differences. Apart from occurring much earlier, obviously, VJ’s damage was less severe. Unlike HM he did not lack the nearby entorhinal cortex or parahippocampal cortex.
The authors followed him up to age 17, and did lots of tests of his cognitive function. The pattern that emerged is that VJ showed a selective impairment of memory for personal events (episodic memory). He learned to read normally, and he scored well on tests of general knowledge. So he had preserved semantic memory, memory for facts. His IQ was normal.
Even his episodic memory impairment was selective, however. He was severely impaired on tests of memory recall, i.e. “What did you do yesterday?”. But on tests of recognition – “Have you ever seen this picture before?” – he did perfectly well.
This fits with lots of previous studies showing that the hippocampus is required for recall while the nearby cortex is more important for recognition. When asked to describe events in his past, he was essentially unable to do so, unless he was provided with “clues” or “reminders” to trigger recognition.
So VJ’s brain couldn’t rewire itself to compensate for the lack of a hippocampus, despite the fact that the damage occurred at birth, and the brain is considered to be at its most plastic during childhood.
This is not all that surprising really. The hippocampus is a unique region, containing specialized circuitry which is just not found anywhere else in the brain. Most of the evidence for large-scale neuroplasticity concerns the cerebral cortex. When part of the cortex is damaged, other cortical areas can sometimes compensate for the loss: but the cortex can’t turn itself a substitute hippocampus.
Bindschaedler, C., Peter-Favre, C., Maeder, P., Hirsbrunner, T., & Clarke, S. (2010). Growing up with bilateral hippocampal atrophy: From childhood to teenage Cortex DOI: 10.1016/j.cortex.2010.09.005