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Theory of Intelligent Design, the best explanation of Origins » Intelligent Design » Neurology » Speech and the Brain

Speech and the Brain

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1 Speech and the Brain on Sat Apr 02, 2016 4:04 pm


Speech and the Brain

Dr. C. George Boeree


The brain is divided into two halves, a left hemisphere and a right hemisphere.  This is called lateralization, and applies to any animal further up the evolutionary tree than, say, a worm.  In animals that are particularly vocal, such as canaries, dolphins, and chimpanzees, it seems that one hemisphere or another is dedicated to controlling those behaviors and the responses to them.  

In human beings, it is the left hemisphere that usually contains the specialized language areas.  While this holds true for 97% of right-handed people, about 19% of left-handed people have their language areas in the right hemisphere and as many as 68% of them have some language abilities in both the left and the right hemispheres.

Lateralization was first discovered in the 1800's by physicians (such as Broca and Wernicke, who we will discuss in a bit) who did autopsies on patients who had had several language difficulties before their deaths.  These physicians found damage to particular areas of the brain now named after them, and these areas were consistently on the left hemisphere. 

These discoveries were later confirmed in the 1950's by researchers, such as Wilder Penfield and Herbert Jasper.  Brain surgery is normally done using only local anesthesia.  The patient is sedated but not unconscious.  This is done in part in order to be able to keep tabs on the patient's experiences.  Penfield and Jasper took advantage of these patients (with their permission, of course) and stimulated certain areas electrically.  When asked questions, the patients were unable to reply during te stimulation of the left hemisphere, but had no problem responding during stimulation of  the right hemisphere.

In the 1960's, another, rather bizarre, set of experiments involved using sodium amytal, a very fast-acting anesthetic.  Researchers were able to put one or the other hemisphere of volunteers to sleep by injecting the anesthetic into either the right or left carotid artery (which supply blood to the same-side hemispheres).  Lo and behold, the patients who had the left hemisphere put to sleep did not respond to questions!

Most recently, researchers have taken advantage of the huge advances made in brain imaging.  In particular, the PET scan ("positron emission tomography") provides a computer with the information needed to construct a three dimensional map of a persons brain including the relative activity of different areas.  PET scans involve injecting someone with a radioactive glucose solution.  Since active areas of the brain use more energy, and therefore more glucose, they release more radiation, which the computer translates into "warmer" colors such as yellow and red.  Areas that are less active are shown with "cooler" colors such as green and blue.  As by now you should expect, certain areas of the left hemisphere were more active while people were engaged in linguistic activities.

Most early studies were done on mature male volunteers.  Since then, scientists have gone on to study female volunteers and even children.  Interestingly, women seem to be slightly less "lateralized" than men, being more likely to use portions of the right hemisphere as well as the left.

Studies of children have provided some fascinating information:  If a child has damage to the left hemisphere, the child may develop language in the right hemisphere instead.  The younger the child, the better the recovery.  So, although the "natural" tendency is for language to develop on the left, our brains are capable of adapting to difficult circumstances, if the damage occurs early enough.

Broca's Area

The first language area within the left hemisphere to be discovered is called Broca's Area, after Paul Broca.  Broca was a French neurologist  who had a patient with severe language problems:  Although he could understand the speech of others with little difficulty, the only word he could produce was "tan."  Because of this, Broca gave the patient the pseudonym "Tan."  After the patient died, Broca performed an autopsy, and discovered that an area of the frontal lobe, just ahead of the motor cortex controlling the mouth, had been seriously damaged.  He correctly hypothesized that this area was responsible for speech production.

Physicians called the inability to speak aphasia, and the inability to produce speech was therefore called Broca's aphasia, or expressive aphasia.  Someone with this kind of aphasia has little problem understanding speech.  But when trying to speak themselves are capable only of slow, laborious, often slurred sequences of words.  They don't produce complete sentences, seldom use regular grammatical endings such as -ed for the past tense, and tend to leave out small grammatical words. 

It turns out that Broca's area is not just a matter of getting language out in a motor sense, though.  It seems to be more generally involved in the ability to deal with grammar itself, at least the more complex aspects of grammar.  For example, when they hear sentences that are put into a passive form, they often misunderstand:  If you say "the boy was slapped by the girl," they may understand you as communicating that the boy slapped the girl instead.

Wernicke's Area

The second language area to be discovered is called Wernicke's Area, after Carl Wernicke, a German neurologist.  Wernicke had a patient who could speak quite well, but was unable to understand the speech of others.  After the patient's death, Wernicke performed an autopsy and found damage to an area at the upper portion of the temporal lobe, just behind the auditory cortex.  He correctly hypothesized that this area was responsible for speech comprehension.

This kind of aphasia is known as Wernicke's Aphasia, or receptive aphasia.  When you ask a person with this problem a question, they will respond with a sentence that is more or less grammatical, but which contains words that have little to do with the question or, for that matter, with each other.  Strange, meaningless, but grammatical sentences come forth, a phenomenon called "word salad."

Like Broca's area is not just about speech production, Wernicke's is not just about speech comprehension.  People with Wernicke's Aphasia also have difficulty naming things, often responding with words that sound similar, or the names of related things, as if they are having a very hard time with their mental "dictionaries."

Other Areas

Despite the fact that Broca's and Wernicke's Areas are in different lobes, they are actually quite near each other and intimately connected by a tract of nerves called the arcuate fascilicus.  There are also people who have damage to the arcuate fascilicus, which results in an aphasia known as conduction aphasia.  These people have it a bit better than other aphasias:  They can understand speech, and they can (although with difficulty) produce coherent speech, they cannot repeat words or sentences that they hear.

Reading and writing are a part of language as well, of course.  But since these skills have only been around a few thousand years, they are not as clearly marked in terms of brain functioning as the basic comprehension and production areas.  But there is an area of the brain called the angular gyrus that lies about halfway between Wernicke's area and the visual cortex of the occipital lobe.  It was discovered, after a young patient with reading problems died and his brain  was examined during autopsy.  The angular gyrus showed significant abnormalities.

The angular gyrus has been implicated in problems such as alexia (the inability to read), dyslexia (difficulties with reading), and agraphia (the inability to write).  In research involving the use of PET scans on people with these problems, the angular gyrus is not as active as it is in other people while engaged in reading or writing.  However, problems such as dyslexia also can involve other areas of the brain, or not involve brain disorders at all.

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2 Re: Speech and the Brain on Sat Apr 02, 2016 7:15 pm


Brain areas involved in speech production 1

The ability to produce accurate speech sounds in rapid succession is something we humans take for granted. In fact, speech production is an extremely involved process. Thoughts must be translated into linguistic representations (itself not a trivial feat), which are then sent to speech mechanisms that can coordinate, initiate, modify and execute the articulation of an utterance. Through the study of patients with disorders affecting this complex process, we have come to learn that numerous brain areas are recruited in speech production and that they hang in a precarious balance that is easily affected by neurological disease and dysfunction.

The coordination of articulatory movements, an end‐stage component of speech production, has received increased attention in recent years. In order for sounds to be produced correctly, the lips, tongue, jaw, velum and larynx must make accurate movements at the right time or the intended sounds become distorted. For example, to say the simple word ‘gap,’ airflow must briefly be halted by raising the back of the tongue to the soft palate. This airflow is suddenly released, during which time the vocal cords must vibrate to create phonation. The tongue and jaw lower and the air should flow unobstructed to produce the proper vowel. The lips seal and the cords relax. All of this must be orchestrated perfectly in time and sequence so that the word ‘gap’ results. Given the many fine movements that are required for speech production, it is no wonder that the mouth area is so largely represented in the homunculus of primary motor cortex.

Patients with deficits in this ability to programme speech movements are said to have a disorder known as ‘apraxia of speech’. The disorder has been well studied in the realm of speech–language pathology, and treatment for the disorder has received equal attention (Wertz et al., 1984; Duffy, 1995; McNeil et al., 1997). The brain regions that might support this function had been less well investigated until the advent of neuroimaging techniques that allowed for the in vivo investigation of the brain areas affected in patients who had sustained injuries that resulted in apraxia of speech. In one such study (Dronkers, 1996), the computer‐reconstructed lesions of 25 chronic stroke patients with left hemisphere lesions who had been diagnosed with apraxia of speech were overlapped to determine if a common area of infarction could be found in this group. The only region of overlap in 100% of the cases was found in the superior tip of the precentral gyrus of the insula (SPGI). Since this region fell within the central‐most area of the brain, it was possible that this common area merely reflected a vulnerable area in patients with left hemisphere strokes and was not specific to apraxia of speech. For that reason, the lesions of 19 patients who were similarly assessed but who did not carry the diagnosis of apraxia of speech were also overlapped. Their lesions spanned the same distribution of the left hemisphere but completely spared the same region that was affected in the patients with the disorder. This dissociation was taken to mean that the SPGI might play some role in the coordination of articulatory movements. Such lesion analysis methods serve not only to tie behaviours to brain areas, but also to take the complementary, reverse step of comparing the behaviour of patients with spared regions of interest. Other patient studies and some functional imaging studies have also implicated the insula in the process of speech production (e.g.Wise et al., 1999; Nestor et al., 2003; Gorno‐Tempini et al., 2004).

In this issue of Brain, the relationship of the insula to apraxia of speech was examined by Hillis and colleagues in acute stroke patients by utilizing diffusion‐weighted imaging (DWI) and perfusion‐weighted imaging (PWI) within the first 24 h after stroke. Forty patients with and 40 without lesions and/or hypoperfusion to the insula were selected and given several short oral language tasks from which a diagnosis of apraxia of speech was later extracted. The authors found no reliable relationship between apraxia of speech and structural changes or low blood flow to regions of the insula, but instead found that 84% of patients with apraxia of speech had such changes in the posterior inferior frontal gyrus. The authors present an interesting and alternative method for identifying the relationship between behavioural deficits and affected regions of the brain, and raise questions concerning the best methods of lesion analysis.

The study of Hillis et al. makes a contribution to the field for several reasons. First, its starting point is the regions of interest that were lesioned and/or dysfunctional and evaluates whether patients with changes there show the expected deficit. This is the complementary approach to first selecting patients with the deficit and then evaluating if they demonstrate a common lesion. Secondly, the study evaluates patients in the acute stage of stroke and captures those who might have small lesions that could resolve quickly and might be overlooked in a study of chronic patients. Thirdly, the study draws on the authors’ earlier work that evaluates both dysfunctional and structural damage within the first 24 h. Few studies have assessed large numbers of patients with both techniques in this early stage after stroke and thus have not evaluated the effects of tissue dysfunction in addition to the effects of tissue loss.

At the same time, the paper opens the discussion concerning the assessment of lesion–symptom mapping in brain‐injured patients. What is the best way to assess which areas are important for certain functions? How do methods of lesion analysis (lesion overlapping, DWI and PWI) contribute to this understanding? How do brain–behaviour relationships in acute patients using one set of methods reliably compare with those found using an alternative method in chronic patients? Should these relationships be pursued in acute patients before the brain has had the opportunity for reorganization of function, or should they be assessed in chronic patients when the physiological effects of the brain injury have passed and the behaviour has settled into a stable pattern? Should we be viewing structural changes or functional ones, and how do they compare? Should we constrain our search to regions of interest or open our investigation to all regions of the brain? Finally, how should behavioural deficits be investigated? Should we try localizing individual symptoms or search for syndromes and networks in the brain?

Clearly all of these approaches contribute to the study of brain–behaviour relationships in complementary ways. The difference in findings between the acute patients of Hillis et al. and the chronic patients of Dronkers is of great interest and questions what might be happening between these two stages that yields a shift in localization between Broca’s area to the precentral gyrus of the insula for speech praxis. The ability to view both functional and structural lesions in the brain allows us to see which areas are recruited during a behavioural task and which ones are necessary to support the function. While lesion overlapping allows us to consider a wide area of brain in our search for localization of particular disorders (and has succeeded in yielding numerous associations throughout the brain, not just those in the insula), the a prioridetermination of regions of interest allows us to focus on the specific deficits that follow injury to that one area. Ideally, a mixture of both techniques would be advantageous and would allow for more detailed correlations between symptoms and brain regions. The new voxel‐based methods such as VLSM (voxel‐based lesion–symptom mapping; Bates et al., 2003) in which well‐defined continuous data can be evaluated at the voxel level are already making contributions in this area (e.g. Saygin et al., 2003; Dronkers et al., 2004)

Speech production is a complex process, involving a networked system of brain areas that each contribute in unique ways. Areas beyond Broca’s area and the anterior insula have been implicated in the complex process of producing speech movements. Future studies, associating even more specific apraxia of speech symptoms (e.g. pure motoric groping) with discrete brain areas, may further our understanding of such a distributed network. For the patients suffering from apraxia of speech, a better characterization of the disorder and its symptoms may ultimately help clinicians in planning for more effective rehabilitation. Perhaps using multiple methods, e.g. lesion overlap, DWI, PWI and functional MRI, to follow brain‐damaged patients from the acute phase through early and late stages of rehabilitation will add to our knowledge of the time course of recovery, localization of function and the nature of reorganization after injury.


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