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When the Brain Goes Wrong
… language disorders do not occur in isolation; aphasic disturbances rarely occur in the absence of memory impairment or attention/executive problems.
Yves Turgeon and Joël Macoir1
ONE WAY TO TEST the prediction that language is innate and hardwired in certain portions of the brain is to examine the nature of language disorders. If language is an encapsulated, innate module of the brain, then it should be possible to observe language problems that are linked exclusively to particular language-only parts of the brain. If, on the other hand, language is a culturally acquired invention, there should be no specifically linguistic disorders. While the latter idea, that there are no heritable, language-only disorders, seems correct, there is a list of respected researchers that claim otherwise. To help determine what the truth really is, the evidence from so-called language-specific disorders needs to be considered here.
The place to begin is the disorder with the challenging label, specific language impairment (SLI). SLI supposedly affects linguistic functions exclusively. No other part of the brain or other aspects of our cognitive functioning is purported to be affected in this syndrome, according to some researchers. Some assert that SLI shows that the brain is genetically hardwired for specific linguistic knowledge, because this eponymous deficit affects only linguistic knowledge.
In fact, this label is misleading because it suggests that something has been found that in fact has never been discovered, namely a disorder that affects only our linguistic abilities. To the contrary this disorder always seems to affect non-linguistic aspects of our cognition as well. Therefore, whatever the nature of such impairments are, they are not language-specific.
Even if SLI existed as described, this would not indicate that there is a portion of the brain hardwired by the genes for language. That is because acquired skills and knowledge can also be affected in addition to language. Factors such as amnesia, blunt force trauma, alcohol and bullets are some of the causes of language disorders. Therefore, the existence of a disorder implies on the surface nothing about whether the ability affected by the disorder is innate or learned. On the other hand, the model that takes language as an innate capacity of humans does predict highly specific language deficits. The view that language is instead an invention, a cultural artefact, predicts that language deficits are no more likely than bread-baking deficits.
And it turns out that the thesis that the brain is a general purpose device predicts exactly what is found. Deficits that affect language are multifaceted. The language effects themselves are never more than a portion of the overall syndrome. Therefore, a more detailed look at a few so-called language deficits is called for. Michael T. Ullman and Elizabeth I. Pierpont, neuroscientists at Georgetown University, define SLI along the following lines:
Specific Language Impairment (SLI) is generally defined as a developmental disorder of language in the absence of frank neurological damage, severe environmental deprivation, or mental retardation … Other terms have also been used … such as developmental dysphasia, language impairment, language learning disability, developmental language disorder, delayed speech and deviant language.
There are researchers who consider SLI a dysfunction or deficit of the ‘language module’ of the brain, the mental capacity exclusively responsible for language. Several explanations of SLI have therefore been phrased in terms of syntax (sentence structure), or phonology (sound structure), or morphology (word structure). These are well-defined submodules or subcomponents of language in some theories. One prediction of SLI might be that a child with this disorder is unable to construct the right types of syntactic tree diagrams mentally, however such structures are implemented in the brain. A linguist might predict that someone could be born without the ability to perform the syntactic operation Merge.
An alternative analysis of this ailment is proposed by Ullman and Pierpont, namely that what is referred to as SLI should instead be understood in terms of a ‘procedural deficit’. This counterproposal claims that ‘a significant proportion of individuals with SLI suffer from abnormalities of this brain network, leading to impairments of the linguistic and non-linguistic functions that depend on it’.2 Moreover, they conclude that Broca’s area, the region of the brain associated with not only grammar but most procedural motor skills and activities, is implicated, along with procedural memory (our ability to remember how to do things in sequences), meaning that although one sees effects in language, the root of SLI is not linguistic per se, but something of a higher order, the memory and procedural learning that underlie many human activities, of which language is but one. In the words of Ullman and Pierpont:
The different structures of the procedural system provide distinct and complementary computational and functional contributions. For example, the basal ganglia are particularly important for learning new procedures, but may be less so for the normal processing of already-learned procedures … So, abnormalities of different structures in the system should lead to different types of impairments of procedural memory.3
Although there are many studies such as the one mentioned here against the existence of SLI, it would be premature to consider the matter settled. But, as of this writing, it can be concluded that SLI offers no support for the idea that grammar or language is innate as opposed to the idea that each is a cultural tool that is malleable, changes over time and is learned afresh by every child as they engage in natural conversations and interactions with other members of their community.
Nevertheless, in a 2014 article in the journal Cell, Steven Pinker and Heather van der Lely take a very different view of SLI. They claim that SLI is ‘highly heritable’ and very specific to language. Heritability of SLI is an interesting observation. It would mean that the deficit comes from some hardwired, genetically preordained ability that can become a disability of malfunctioning genes.
But other work has argued that the heritability of SLI may be little more than a gleam in the eye of the beholder. How you define a disease can determine what you find. One study of this kind concludes that: ‘Heritability estimates for specific language impairment (SLI) have been inconsistent … a recent report from the Twins Early Development Study found negligible genetic influence.’4
Moreover, what is inherited is wider than merely a language disorder. Other aspects of cognition are affected. This means that the genetic problem is not so much linguistic as a more general problem of brain processing. The evidence that SLI is a more general malady is just what would be predicted if there were no brain module for language, as the evolutionary record seems to suggest.
As others put it:
The choice of a particular assessment method, the selection of evaluation tools as well as the interpretation of results are highly dependent not only on the clinician’s own conception of language but also on the reference to an assessment model … language disorders do not occur in isolation; aphasic disturbances rarely occur in the absence of memory impairment or attention/executive problems … Language production and comprehension are complex cognitive skills which should not be considered in isolation in assessment procedures.5
Another problem that affects human language is a complete or partial inability to speak, referred to as aphasia, from the Greek a ‘without’ and phasis ‘speech’. Aphasia is caused by brain damage and regularly affects about one million people in the USA alone. Its primary cause seems to be a problem with blood flow to the brain, which is often the by-product of a stroke.*
People with aphasia manifest one of a few different kinds of disorders. They can have problems with understanding what they hear (auditory comprehension) or difficulties communicating intelligibly, find reading and writing challenging or struggle to express themselves verbally. Aphasia is most commonly a result of extensive damage to the left hemisphere, the side of the brain long known to be implicated heavily in language and other tasks. Since the left hemisphere is, however, not exclusively dedicated to lang
uage, this means that aphasia will never affect language only. Some approaches to aphasia in the past have seen it largely in anatomical terms, localising it to what were considered once to be language specific regions of the brain, such as Broca’s and Wernicke’s areas. And indeed it is correct that there are specific kinds of aphasia associated with these general regions in the brain, as we have seen. Broca’s aphasia, also known as ‘motor aphasia’ or ‘expressive aphasia’, is characterised by relatively solid comprehension, but difficulty in speaking. Significantly, however, people with this form of aphasia also usually have paralysis, or at least weakness, in their right appendages – the arm, the leg, or both.
Another well-known type of aphasia is Wernicke’s aphasia, also known as ‘receptive aphasia’ or ‘sensory aphasia’. In this form of aphasia, the subject is able to speak fluently but unable to understand what is said to them. Moreover, their ‘fluent’ speech often is chock-a-block with abnormalities, such as nonsense words that, while fitting the sound patterns of their native language, mean nothing and are otherwise not words at all. There are other forms of aphasia. This is, of course, unsurprising, since there are many aspects of language and many ways in which one might imagine it breaking down, especially if it is an artefact.
In an article in the journal Aphasiology, Edward Gibson and his co-authors offer an instructive analysis of strategies for overcoming aphasic language comprehension problems developed by the aphasics themselves.6 What this team discovered is reminiscent of a G1 language. The aphasics in Gibson’s study use contextual clues more extensively than non-aphasic subjects in order to interpret what is spoken to them. Homo erectus, in my model at least, would have produced utterances that were highly ambiguous or vague or both, depending on his or her interlocutor’s ability to link speech to context for an interpretation more or less in the ballpark of what was intended.† Homo erectus might, therefore, have used a strategy similar to aphasics for interpreting sentences. But that is what all people do. All utterances are interpreted at least in part based on knowledge of culture, the context and the world.
A discussion of language and the brain cannot end, however, before discussing another set of cognitive disorders, collectively known as autistic spectrum disorder. ASD reveals the importance of the society to language and the role of conversation as the apex of linguistic experience. Therefore, we must take special care in our discussion here. Richard Griffin and Daniel C. Dennett of Tufts University get at what seems to be the general thread running through many autism cases, namely that sufferers of autism share a ‘pervasive bias to attend toward local rather than global features’. This is sometimes referred to as ‘weak central coherence’ and means that sufferers struggle to grasp an entire social situation in context.7
The first two people I can remember with ASD were friends of mine. One was a fellow redhead, brother of a grammar-school buddy. The other was a second cousin.
In the case of my friend’s brother, I did not even know of his existence until I visited my friend’s house and learned that he had a brother visiting from another school somewhere. He didn’t seem old enough to be in college, so I couldn’t really understand why he wouldn’t be in school with us. As we were introduced, though, he was quiet and looked around erratically. I was about twelve years old. He would have been perhaps fourteen. He wouldn’t answer me, so I asked my friend, ‘Hey, what’s wrong with your brother? Is he simple-minded?’ My friend laughed. ‘No, he is not simple. He’s pretty smart. Wanna see?’ I immediately replied, ‘Yes!’ though I was curious as to how my friend’s brother would demonstrate his intelligence.
This was answered quickly. My friend took the annual calendar off of his bedroom wall and handed it to me. He suggested that I pick any month and ask his brother what day of the week any date was. ‘What for?’ ‘Just ask him, you’ll see.’ So I thumbed through the calendar and picked a date earlier in the year. I think I asked, ‘What is the day of January 21, 1963?’ He immediately and correctly responded with the day of the week. I ran through about twenty dates all over the year. Then I asked him about other years. He never hesitated; he never erred. I was ready to acknowledge his intelligence as far exceeding my own. My friend’s brother was giggling and giggled harder with every new date I asked him. In my twelve years, I had never heard of anything like that, much less witnessed such an example. ‘How the hell’s he do that?’ I demanded. ‘No idea,’ replied my friend. He told his brother, ‘Great job!’
I learned through this – though only later in life as I continued to think about what I had seen – that my friend’s brother had at least two unusual characteristics: a seemingly deficient social ability and a brain that could do some things better than I had ever seen done. Yet the social difficulty meant that he struggled to carry on a conversation. My friend was particularly solicitous of his brother. ‘He’s done now,’ he announced. ‘Let’s go.’ And so we did.
My next encounter with what, in retrospect, was most probably also ASD was with a second-cousin I used to see daily at school. Other children teased him mercilessly. Once he yelled back at a tormentor with a nearly inarticulate, ‘No, goddamn it!’ and started hitting them with both hands. They initially started laughing. Then they realised he was really hurting them, so they apologised. My cousin stopped and walked away without another word. Neither I nor any of my friends at that time had a concept of neurodiversity. Anyone who didn’t behave exactly as we expected we considered ‘handicapped’.
So if I thought about my cousin, I felt pity for him. Then, one day, in an assembly of the entire junior high school that we both attended, the principal began to announce awards. Eventually he worked his way down the list to the two main awards of the year, scholarship and citizenship. When he said, ‘For the first time both awards go to the same person,’ I wasn’t surprised. I expected them to go to a good friend of mine. But no. The name called, to my amazement, was my cousin’s. For the first time in my life I realised that I was no judge of character. I teared up because I knew all the grief that my cousin put up with every day at school and he won citizenship! Conversations were just excruciatingly difficult for him. When he did talk, he became emotional and inarticulate very quickly. But he went to school. He ate alone. And then he impressed everyone with his intelligence and kindness.
There is, in fact, no single disease or aetiology that corresponds to what the general public calls ‘autism’, only a set of symptoms that professionals have decided to group under the general label of autistic spectrum disorder. Not everyone with this disorder behaves the same, as in the two different examples from my childhood. The symptoms of ASD include the following, broken into a couple of distinct areas:‡
Communication: Autism sufferers struggle with communication and interactions with other people. People with this condition abnormally engage in routines or repetitive behaviours, sometimes called stereotyped behaviours. Autistics do not respond to their names by twelve months of age and cannot easily explain what they want. Generally those with autism do not follow directions. Sometimes they seem to hear, but not at other times. In general those with autism neither point nor wave ‘bye-bye’.
Social Behaviour: People with autism generally don’t smile when smiled at, make poor eye contact and appear to prefer to play alone. When fetching items or picking things up, they generally bring things for themselves only. Autism sufferers are independent for their age, yet give the impression of being in their ‘own world’. They act as if they tune people out and are uninterested in other children, failing to point out interesting objects by fourteen months of age, a normal time frame for that development, and don’t like to play ‘peek-a-boo’. Sufferers do not try to attract their parents’ attention.
Stereotyped Behaviour: Affected individuals get ‘stuck’ doing the same things over and over and can’t move on, showing unusual attachments to toys, objects, or routines (always holding a string or having to put on socks before pants), and spend a lot of time lining things up or putting things
in a certain order. They repeat words or phrases; sometimes called echolalia.
Other Behaviour: Children with autism may not play ‘make believe’ or pretend by eighteen months of age. They have odd movement patterns and do not know how to play with toys appropriately, in spite of being attached strongly to them. Autism sufferers do some things ‘early’ compared to other children, such as walking on their toes, but do not like to climb on things such as stairs. These children don’t imitate silly faces and seem to stare at nothing or wander around with no purpose. They throw intense or violent tantrums. Autistics may be overly active, uncooperative, or resistant and are overly sensitive to noise. The affected also prefer not to be swung or bounced on their parent’s knee, etc.
A variety of causes have been proposed for ASD, including bad socialisation, bad parenting, bad genes, neurological developmental problems, excess testosterone and ‘mind-blindness’ (the purported lack of a theory of mind, that is a failure to recognise that others have a mind like the subject does). Research often produces messy results, though researchers often prefer elegant results. The idea that ASD is caused by ‘mind-blindness’ is a neat generalisation, but just doesn’t seem to get an account of the spectrum of autistic disorders. None of these do. Rather, there is a sense in which they each play a role to a greater or lesser degree. As Dr Helen Tager-Flusberg, one of the world’s leading autism researchers, puts it, ‘Autism is a complex and heterogeneous disorder that should not be reduced to a single underlying cognitive impairment.’8
My own peculiar perspective on ASD as an outsider to the research and lacking the clinical expertise of real professionals, is that it is a breakdown of the ability to build components of the dark matter of the mind, structured cultural knowledge that underlies the development of the psychology of each individual as a cultural being. In other words, I agree with the general assessment in the literature that ASD is at root a social problem. But it is certainly a very unusual type of social problem, one which affects the ability to properly understand the intentions and thinking of others or to structure understanding about others from a background of cultural knowledge.
How Language Began Page 19
