TEMPORAL lOBE
Our student team includes: Julia Parker, Jaime Lynch, Corey Fisher,
Christine Alquisira, and Ann Serene.
In our second project, we will explore the workings of the brain by
exploring the effects of a tumor or a lesion in the temporal cortex
area of the brain responsible for language. The data presented has
been researched by each member of the team and is taken from several
different prospectives.
Julia Parker
From the prospective of the neurologist
Speech and language functions are of fundamental human
significance, both in social practice and in private intellectual
life. When they are disturbed as a consequence of brain disease,
the resultant functional loss exceeds all others in gravity even
blindness, deafness, and paralysis. The neurologist is concerned
with all derangements of speech and language, including those of
reading and writing, because they are the source of great disability
and are almost invariably manifestations of disease of the brain.
In a narrower context, language is the means whereby patients
communicate their complaints and problems to the physician and at
the same time the medium for all delicate interpersonal
transactions. Therefore any disease process that interferes with
speech or the understanding of spoken words touches the very core of
the physician-patient relationship.
Finally, the clinical study of language disorders serves to
illuminate the abstruse relationship between psychological functions
and the anatomy and physiology of the brain.
Languages mechanisms fall somewhere between the well-localized
sensorimotor functions and the more widely distributed complex
mental operations such as imagination and thinking, which cannot be
localized.
Carl Wernicke, of Breslau, more than any other person is
credited with the anatomic-psychologic scheme upon which many
contemporary ideas of aphasia rest. Wernicke's research proves that
there are two major anatomic loci for language. One, an anterior
locus, in the posterior part of the inferior frontal lobe (Broca's
area), in which were contained the "memory images" of speech
movements, and two the insular region and adjoining parts of the
posterior perisylvian cortex, in which were contained images of
sounds. Wernicke's beliefs are that the fibers between these
regions run in the insula and mediated the psychic reflex arc
between the heard and spoken word. Wernicke comprehensive
description of the receptive or sensory aphasia points out four main
features. (1) a disturbance of comprehension of spoken language and
(2) of written language (alexia), (3) agraphia, and (4) fluent
paraphasic speech. He theorized that a lesion interrupting the
connecting fibers between the two cortical speech areas would leave
the patient's comprehension undisturbed but would prevent the intact
sound images from exerting an influence on the choice of words.
Today this is referred to as deep aphasia(Martin and Saffron). This
anatomic scheme is the basis of Wernicke's classification of
aphasia.
Careful case analyses since the time of Broca and Wernicke have
repeatedly documented an association between the receptive
(Wernicke) type of aphasia and lesions in the posterior perisylvian
region and between a predominantly (Broca) motor aphasia and lesions
in the posterior part of the inferior frontal convolution and the
adjacent motor, insular, and opercular regions of the cortex. The
lesion in these cases most often lie in the parietal operculum,
involving the white matter deep to the supramarginal gyrus, where it
presumably interrupts the arcuate fasciculus and posterior insular
subcortex.
The conventional teaching is that there are four main language
areas, situated, in most persons, in the left cerebral hemisphere.
Two are receptive and two are executive. The two receptive areas are
closely related and embrace what may be referred to as the central
language zone. One, subserving the perception of spoken language,
occupies the posterior-superior temporal area and Heschl's gyri. A
second area, subserving the perception of written language, occupies
the angular gyrus in the inferior parietal lobule, anterior to the
visual receptive areas. The supramarginal gyrus, which lies between
these auditory and visual language "centers" and the inferior
temporal region, just anterior to the visual association cortex, are
probably part of this central language zone as well.
The dominance of one hemisphere, usually the left emerges with
speech and the preference for the right hand, especially for
writing, and a lack of development or loss of cerebral dominance as
a result of disease deranges both these traits.
Moreover, the utterances we use to express joy, anger, and fear
are retained even after destruction of all the language areas in the
dominant cerebral hemisphere. The neural arrangements for this
paralinguistic form of communication (intonation, exclamations,
facial expressions, eye movements, body gestures), which subserves
emotional expression, are bilateral and symmetrical and do not
depend solely on the cerebrum.
Propositional, or symbolic, language differs from emotional
language in several ways. Instead of communicating feelings, it is
the means of transferring ideas from one person to another, and it
requires in its development the substitution of a series of sounds
or marks for objects, persons, and concepts. This is the essence of
language. It is not instinctive but learned and is therefore
subject to all the modifying social and cultural influences of the
environment. However, the learning process becomes possible only
after the nervous system has attained a certain degree of
development.
Although speech and language are closely interwoven functions,
they are not strictly synonymous. A derangement of language
function is always a reflection of an abnormality of the brain and,
more specifically, of the dominant cerebral hemisphere. A disorder
of speech may have a similar orgin, but not necessarily, it may be
due to abnormalities in different parts of the brain.
Language function involves the comprehension, formulation, and
transmission of ideas and feelings by the use of conventionalized
signs, marks, sounds, and gestures and their sequential ordering
according to accepted rules of grammar.
Speech, on the other hand, refers more to the articulatory and
phonetic aspects of verbal expression. Thus it appears that human
language function depends upon the integrity of an anatomic region
that embraces the primary receptive areas of the temporal and
occipital lobes (and their association areas in the parietal and
temporal lobes) and the motor areas in the inferior frontal lobe of
the dominant hemisphere.
Wernicke's Aphasia
This syndrome comprises two main elements: one, an impairment
in the comprehension of speech, basically an inability to
differentiate word elements or phonemes, both spoken and written
which reflect involvement of auditory association areas or their
separation from the primary auditory cortex (transverse gyri of
Heschl. And two, a relatively fluent but paraphasic speech, which
reveals the major role of the auditory region in the regulation of
language.
The defect in language is manifest further by a varying
inability to repeat spoken and written words. The involvement of
visual association areas or their separation from the primary visual
cortices is reflected in an ability to read (alexia). The patient
talks volubly, gestures freely, and appears strangely unaware of his
deficit. Speech is produced without effort, the phases and
sentences appear to be of normal length and are properly intonated
and articulated. Despite the fluency and normal prosody, the
patient's speech is remarkably devoid of meaning.
In contrast to Broca's aphasia, the patient with Wernick's
aphasia produces many nonsubstantive words and the words themselves
are often malformed or inappropriate, a disorder referred to as
paraphasia. A phoneme (the minimum unit of sound that permits the
differentiation of the meaning of a word (for example: "The grass is
greel"); this is called literal paraphasia. The substitution of one
word for another ("The grass is blue") is called verbal paraphasia,
or semantic substitution. Neologisms for example, phonemes,
syllables, or words that are not part of the language may also
appear ("The grass is grumps").
Fluent paraphasia speech may be entirely incomprehensible
(gibberish). Fluency is not an invariable feature of Wernicke's
aphasia. Speech may be hesitant, in which case the block tends to
occur in part of the phase. The patient with such a disorder
conveys the impression of constantly searching for the correct word
and of having difficulty in finding it.
Although the motor apparatus required for the expression of
language may be quite intact, patients with Wernicke's aphasia are
unable to function as social organisms because they are deprived of
all means of communication. They cannot understand what is said to
them; a few simple commands may still be executed, but there is
failure to carry out complex ones. They cannot read aloud or
silently with comprehension, tell others what they think, or write
spontaneously. Written letters are often combined into meaningless
words, but there may be a scattering or correct words. In trying to
designate an object that they can see or feel, they cannot find the
name, even though they can sometimes repeat it from dictation; nor
can they write from dictation the very words that they can copy.
The copying performance is notably slow and laborious and conforms
to the contours of the model, including the examiner's handwriting
style. All these defects, of course, may be present in varying
degrees of severity. In general, the defects in reading, writing,
naming, and repetition parallel in severity the defect in
comprehension.
There are, however, exceptions in which either reading or the
understanding of spoken language is more affected. Some
aphasiologists thus speak of two Weinicke syndromes. In terms of
the Wernicke schema, the motor language areas are no longer under
control of the auditory, visual and other referent areas. The term
referent designates the cortical area in the posterior perisylvian
region, where visual, tactile, and auditory memories for words are
integrated. The referent centers are also integrated with the motor
language area, allowing the expression of self-generated verbal
thoughts. The language disturbance caused by lesions in the
referent centers was called central aphasia both by Brain and by
Goldstein.
The disconnection of the motor speech areas from the auditory,
visual and other referent centers accounts for the impairment of
repetition and the inability to read aloud. Reading may remain
fluent, but with the same paraphasia errors that mar conversational
language.
The occurrence of dyslexia (visual perception of letters and
words) with lesion in the temporal lobe is explained by the fact
that most individuals learn to read by transforming the printed word
into the auditory form before it can gain access to the referent
centers.
Only in the congenitally deaf is there thought to be a direct
pathway between the visual and referent centers.
Wernicke's aphasia that is due to stroke usually improves in
time, sometimes to the point where the deficits can be detected only
by asking the patient to repeat unfamiliar words from dictation, to
name unusual objects or parts of objects, to spell difficult words,
or to write complex self-generated sentences. A more favorable
prognosis attends those forms of Wernicke's aphasia in which some of
the elements, for example; reading, are only slightly impaired.
As a rule, the lesion lies in the posterior perisylvuian region
(comprising posterosuperior temporal, opercular supramarginal,
angular, and posterior insular gyri) and is usually due to embolic
(less often thrombotic) occlusion of the lower division of the left
middle cerebral artery. A hemorrhage confined to the subcortex of
the temporoparietal region or involvement of this area by tumor,
abscess, or extension of small pataminal or thalamic hemorrhage may
have similar effects but a different prognosis.
A lesion that involves structures deep to the posterior
temporal cortex will cause an associated homonymous hemianopia.
Sometimes there are no associated neurologic signs; and the aphasia
patient may be misdiagnosed as psychotic, especially if there is
jargon aphasia. The posterior perisylvian region appears to
encompass a variety of language functions, and seemingly minor
changes in size and locale of the lesion are associated with
important variations in the elements of Wernicke's aphasia or lead
to conduction aphasia or to pure word deafness.
The interesting theoretical problem is whether all the
deficits observed are indicative of a unitary language function that
resides in the posterior perisylvian region or, instead, of a series
of separate sensorimotor activities whose anatomic pathways happen
to be crowded together in a small region of the brain.
REFERENCES
Brian, R. & Goldstein,K.,1941:The significance of the frontal lobes
for mental performance, J. Neurol Psychopathol
Carlson,N.2001:Physiology of Behavior, 7th Edition,Allyn and Bacon,
Needham Heights, MA.
Gardiner,AH, 1979: The Theory of Speech and Language.Greenwood
Press, Westport, CN.
Goetz MD., Christopher & Weiner MD.,William, 1998:Neurology for the
Non- Neurologist,Third Edition, J.B. Lippincott Company,
Philadelphia,PA.
Kertesz, A. 1989:Aphasia and Associated Disorders. Allyn and Bacon,
Needham Heights, MA.
Saffran,Martin EM 1990:A connectionist account of deep aphasia.
Brain Language 43:240
Jaime Lynch
Neurosurgeon's View
Auditory receptive aphasia is also known as auditory sensory
aphasia, auditory agnosia, and Wernicke's aphasia. In its pure form
it is characterized by loss of the ability to comprehend the
significance of spoken words in the absence of deafness (Haerer,
1992). Wernicke's fluent aphasia is usually seen with dominant
temporal lobe disease in the form of cerebrovascular accidents or
sometimes tumors. The rapid onset in an elderly individual suggests
the former, whereas a more indolent course can be seen with tumors.
When the speech pattern is encountered, the clinician should
immediately focus attention on the dominant temporal lobe.
Associated findings often include the superior quadrant anopia, and
temporal lobe seizures may be an associated phenomenon (Weiner,
1994).
The three cortical levels for the reception and interpretation
of the auditory impulses are not as clearly defined as those for the
reception and interpretation of visual impulses. Areas 41 and 42,
located in the traverse temporal gyri (Heschl's convolutions) on the
dorsal surface of the posterior portion of the superior temporal
convolution, are probably the centers for both primary reception and
recognition of auditory impulses. Lesions of areas 41 and 42, or
the regions immediately surrounding them, may cause a general
auditory agnosia in which the patient loses his ability to recognize
or interpret ordinary sounds, such as the ringing of a bell, and
also his memory for them. This is psychic deafness; there may also
be loss of "reauditorization" of sounds. Owing to the fact that
auditory impulses pass to both temporal lobes and there is little
unilateral cerebral dominance for ordinary sounds, there is never
any marked disability, either deafness or complete auditory agnosia,
with unilateral temporal lobe lesions (Haerer, 1992).
Wernicke's area, which occupies a crescentic zone in the
posterior third of the superior temporal convolution of the dominant
hemisphere, just lateral to the transverse temporal gyrus of Heschl,
has been called the center for the recognition, interpretation, and
recall of word symbols and their association as a function of
language. A lesion at this site may cause an auditory receptive
aphasia, auditory verbal agnosia, or word deafness. There is loss
of ability to comprehend the significance of spoken words or recall
their meaning: the patient can still hear and can recognize voices,
but not the words they utter, and he cannot repeat what he hears.
He can read without difficulty, and may be able to speak normally,
but the loss of ability to comprehend the significance of spoken
words includes those spoken by the patient himself as well as by
others, so that there is usually a syntactical defect, or inability
to arrange words in proper sequence, accompanied by the employment
of incorrect or unintelligible words, unconventional and gibberish
sounds, and senseless combinations. The patient is not aware of his
errors in speaking. The resulting misuse of words and defect of
sequence is termed agrammatism, paraphasia, or jargon aphasia. He
may be able to repeat what others have said even though he does not
understand the meaning. Word deafness occasionally is congenital
(Haerer, 1992).
In acute Wernicke syndrome, the EEG may show diffuse slowing,
or it may be normal. CSF is normal except for occasional mild
protein elevation. Elevated blood pyruvate, falling with treatment,
is not specific. Decreased blood transketolase (which requires
thiamine pyrophosphate as cofactor) more reliably indicates thiamine
deficiency (Tierney, 2000). Radiography of the chest may reveal
cardiomegaly or valvular calcification; the presence of a neoplasm
would suggest that the neurologic deficit is due to metastasis
rather than stroke. A CT scan of the head (without contrast) is
important in excluding cerebral hemorrhage, but it may not permit
distinction between a cerebral infarct and tumor. CT scanning is
preferable to MRI in the acute stage because it is quicker and
because intracranial hemorrhage is not easily detected by MRI within
the first 48 hours after a bleeding episode. In selected patients,
carotid duplex studies, MRI and MR angiography, and conventional
angiography may also be necessary. Diffusion-weighted MRI is more
sensitive than standard MRI in detecting cerebral ischemia (Tierney,
2000).
Wernicke disease constitutes a medical emergency, and the
recognition (or even the suspicion of its presence) demands the
immediate administration of thiamine. The prompt use of thiamine
prevents progression of the disease and reverses those lesions that
have not yet progressed to the point of fixed structural change. In
patients who show only ocular signs and ataxia, the administration
of thiamine is crucial in preventing the development of an
irreversible amnesic state (Adams, 1997).
Untreated Wernicke syndrome is fatal, and the mortality rate
is 10 percent among treated patients (Tierney, 2000). Patients who
die in the acute stages of Wernicke disease show symmetrical lesions
in the paraventricular regions of the thalamus and hypothalamus,
mammillary bodies, periaqueductal region of the midbrain, floor of
the fourth ventricle, and superior cerebellar vermis. Lesions are
consistently found in the mammillary bodies, less consistently in
other areas. The microscopic changes are characterized by varying
degrees of necrosis of parenchymal structures, though it is seldom
complete. The tissue appears loose and vacuolated. Within the area
of necrosis, nerve cells are lost, but usually some remain; some of
these are damaged but others are intact. Myelinated fibers are more
affected than neurons. These changes result in a prominence of the
blood vessels, although in some cases there is a true endothelial
proliferation. In the areas of parenchymal damage there is
astrocytic and microglial proliferation. Discrete hemorrhages were
found in only 20 percent of the cases, and many of them appear to be
agonal in nature. The cerebellar changes consist of a degeneration
of all layers of the cortex, particularly of the Purkinje cells;
usually this lesion is confined to the superior parts of the vermis,
but in advanced cases the cortex of the most anterior parts of the
anterior lobes is involved as well (Adams, 1997).
Adams, R. D., Victor, M., & Ropper, A. H. (1997). Principles of
neurology (6th ed.). New York: McGraw-Hill.
Haerer, A. F. (1992). The neurologic examination (5th ed.).
Philadelphia: J. B. Lippincott.
Tierney, L. M., Jr., M.D., McPhee, S. J., M.D., & Papadakis, M. A.,
M.D. (Eds.). (2000). Current medical diagnosis and treatment (39th
ed.). New York: McGraw-Hill.
Weiner, W. J. & Goetz, C. G. (1994). Neurology for the non-
neurologist (3rd ed.) Philadelphia: J. B. Lippincott.
Corey Fisher
Wernicke's aphagia from the neurologist's perspective
Within the region of the brain known as Wernicke's area, there
lie separate neural subsystems. These subsystems each perform a
very specific function that makes auditory association possible.
These specific subsystems perform such tasks as recognizing the
spoken word, comprehending the meaning of words, and the process of
converting our own thoughts into words. Wernicke's aphagia can
therefore be classified by the exhibition of these symptoms.
The role of a neurologist is to diagnose and treat diseases of
the nervous system. In the case of Wernicke's aphagia, (and its
different forms), the neurologist must determine exactly which part
of Wernicke's area is damaged by assessing the patient's
comprehension capabilities. Since two specific areas in the brain
must be damaged for Wernicke's aphagia to occur, it is useful to
examine the disorders that occur when each of these two subsystems
are damaged individually.
Symptoms such as the inability to comprehend the spoken word,
the written word, as well as the inability to understand what one's
self is saying or writing, is characteristic of pure word deafness
(Carlson, 1998, p.485). This specific type of aphagia can be
assessed by examining the patient's ability to distinguish between
different vowel sounds. Studies have shown that people who are
afflicted with pure word deafness can still distinguish different
vowel sounds, but generally cannot distinguish the different
consonants from one another. Stop consonant sounds such as /t/,
/d/, /k/, and /p/, are especially difficult for people with pure
word deafness to separate; while consonants with a longer duration
such as /s/, /z/, and /f/ are usually easier for them to distinguish
(Carlson, 1998,p.485).
Pure word deafness can be caused by injury to one of two
areas. The first is damage to Wernicke's area itself, and the
second is bilateral damage to the primary auditory cortex. Damage
to either of these two parts of the system will result in the
disruption of the analysis of the sounds of words and thus the
prevention of the patient's ability to comprehend the attempt at
communication (Carlson, 1998, p.486). In order for the neurologist
to distinguish which part of the brain is actually damaged in this
case, a PET scan or MRI must be performed.
However, in some cases people who are afflicted with pure word
deafness can understand what other people are saying by reading
their lips. Some other people with this same affliction can also
read and write with comprehension. What this suggests is that pure
word deafness, is not an inability of the patient to comprehend word
meaning, but rather an inability of the patient to be able to
distinguish the sounds of real words from those of
psuedowords(Carlson, 1998, p.486).
"Wernicke's area, localized to the posterior part of the left
superior temporal gyrus (STG), stores the encoded memories of
familiar heard words, from which there is access to both meaning and
speech production,"(Wise, 2001, p.83). When damage extends past
Wernicke's area into the region that surrounds the lateral fissure,
(at the junction of the occipital, temporal, and parietal lobes),
the other symptoms of Wernicke's aphagia that are not present in
pure word deafness now become apparent (Carlson, 1998, p.487).
Damage to this area around the lateral fissure alone causes patients
to suffer from what is called transcortical sensory aphagia (TSA).
Patient's with this disorder, unlike pure word deafness or complete
Wernicke's aphagia, can repeat what other people say to them, but
they cannot comprehend the meaning of what they are hearing. This
means that people suffering from TSA can recognize words with no
problem, but cannot understand the words that they are hearing nor
can they produce meaningful speech of their own.
Transcortical sensory aphagia and pure word deafness clearly
illustrate that there are different subsystems that are involved in
Wernicke's aphagia. "The sparing of repetition distinguishes TSA
from other receptive aphagias and agnosias, including Wernicke's
aphagia and pure word deafness" (Boatman, 2000, p.1634). The
symptoms of Wernicke's aphasia are a combination of both TSA and
pure word deafness, and therefore both of the regions involved in
those must be damaged in order for Wernicke's aphagia to be
diagnosed.
The neurologist working with a patient that has what seems to
be Wernicke's aphasia must make sure that all, and not just some, of
the symptoms of Wernicke's aphagia are exhibited by their patient
before making their diagnosis. Symptoms of pure word deafness must
then be assessed via consonant and vowel recognition trials, and
symptoms of transcortical sensory aphagia must also be evident.
REFERENCES
Carlson, N.R.(1998). Physiology of Behavior (6thed.).Needham Heights:
Allyn and Bacon.
Wise, R.J.S., Scott, S.K., Blank, S.C., Mummery, C.J., Murphy, K.,
Warburton, E.A. (2001). Separate neural subsystems within
'Wernicke's area'. Brain, 124, 83-95.
Boatman, D., Gordan, B., Hart, J., Selnes, O., Miglioretti, D.,
Frederick, L. (2000). Transcortical sensory aphagia: revisited and
revised. Brain, 123, 1634-1642.
Christine Alquisira
Temporal Lobes--Wernicke's Area
Perspective of the Patient
Temporal Lobes, Functions, and Symptoms of Damage:
The temporal lobes of the brain (located just above the ears) are
responsible for performing certain functions such as hearing
ability, memory acquisition, some visual perceptions and the
categorization of objects. Kolb & Wishaw (1990) have identified ten
principle symptoms of temporal lobe damage: 1) Difficulty in
recognizing faces (Prosopagnosia), 2) Difficulty in understanding
spoken words (Wernicke's Aphasia), 3) Disturbance with selective
attention to what one sees and hears, 4) Difficulty with
identification of, and verbalization about objects, 5) Short-term
memory loss, 6) Interference with long-term memory, 7) Increased or
decreased interest in sexual behavior, 8) Inability to categorize
objects (Categorization), 9) Right lobe damage can cause persistent
talking and lastly, 10) Increased aggressive behavior.
Selective attention to visual or auditory input is common with
damage to the temporal lobes (Milner, 1968). Left side lesions
result in decreased recall of verbal and visual content, including
speech perception. Right side lesions result in decreased
recognition of tonal sequences and many musical abilities. Right
side lesions can also effect recognition of visual content (e.g.
recall of faces).
The temporal lobes are also involved in the primary
organization of sensory input (Read, 1981). Individuals with
temporal lobes lesions have difficulty placing words or pictures
into categories.
Language can be effected by temporal lobe damage. Left temporal
lesions disturb recognition of words. Right temporal damage can
cause a loss of inhibition of talking.
The temporal lobes are highly associated with memory skills.
Left temporal lesions result in impaired memory for verbal material.
Right side lesions result in recall of non-verbal material, such as
music and drawings.
Seizures of the temporal lobe can have dramatic effects on an
individual's personality. Temporal lobe epilepsy can cause
perseverative speech, paranoia and aggressive rages (Blumer and
Benson, 1975). Severe damage to the temporal lobes can also alter
sexual behavior (e.g. increase in activity) (Blumer and Walker,
1975).
Wernicke's Area and Aphasia
The Wernicke's Area is a region of the auditory association
cortex on the left temporal lobe of humans, which is important in
the comprehension of words and the production of meaningful speech.
A lesion to this area can produce a condition called Wernicke's
aphasia. The primary characteristics of this condition are poor
speech comprehension and production of meaningless speech. Unlike
Broca's aphasia (a form of aphasia characterized by agrammatism,
anomia and extreme difficulty in speech articulation) Wernicke's
aphasia is fluent and unlabored; the person does not strain to
articulate words and does not appear to be searching for them.
(Carlson 1998)
The patient maintains a melodic line, with the voice rising and
falling normally. When one listens to the speech of a person with
Wernicke's aphasia, it appears to be grammatical. That is, the
person uses function words such as 'the' and 'but' and employs
complex verb tenses and subordinate clauses. However, the person
uses few content words, and the words that he or she strings
together just do not make sense. In the extreme, speech
deteriorates into a meaningless jumble.
A remarkable fact about people with Wernicke's aphasia is that
they often seem unaware of their deficit. That is, they do not
appear to recognize that their speech is faulty, nor do they
recognize that they cannot understand the speech of others. One
person with Wernicke's aphasia made the following responses when
asked to name ten common objects: toothbrush=stokery,
cigarette=cigarette, pen=tankt, knife=nike, fork=fahk, quarter=
minkt, pen=spentee, matches= senktr, key=seek, and comb=sahk.
(Carlson, 1998).
Wernicke's Aphasia: Analysis
Because the superior temporal gyrus is a region of auditory
association cortex, and because a comprehension deficit is so
prominent in Wernicke's aphasia, this disorder has been
characterized as a receptive aphasia. Wernicke suggested that the
region that now bears his name is the location of memories of the
sequences of sounds that constitute words. This hypothesis suggests
that the auditory association cortex of the superior temporal gyrus
recognizes the sounds of words, just as the visual association
cortex of the inferior temporal gyrus recognizes the sight of
objects.
Tests--CT scans, MRI'S, and more:
Common tests for temporal lobe functions are: Rey-Complex
Figure (visual memory) and Wechsler Memory Scale - Revised (verbal
memory). In traumatic brain injury the brain may be injured in a
specific location or the injury may be diffused to many different
parts of the brain. It is this indefinite nature of brain injury
that makes treatment unique for each individual patient. In the past
twenty years, a great deal has been learned about brain function,
and we learn more everyday. We can make guesses about the nature of
the problems an individual may have from knowing the location of a
lesion. Diagnostic procedures such as CT scans and MRI'S can also
provide information about a brain injury.
Functional imaging of the brain demonstrates that this highly
complex organ adapts to injury by redistributing its cognitive
workload across established neural networks and recruiting local
cortical areas to fill in for lost functions like speech and
language comprehension.
"Functional MRI [magnetic resonance imaging] indicates that the
dogma that some areas of the brain are not important for normal
function is clearly fallacious," said Dr. Keith Thulborn, director
of MR research at the University of Illinois at Chicago at the
annual meeting of the American Association for the Advancement of
Science in San Francisco. "Loss of any brain tissue is likely to
compromise the reserve capacity of many large-scale neurocognitive
networks that will ultimately be reflected in the performance of
more difficult tasks or recovery from subsequent disease processes."
Watching the brain at work with a very-high-field MRI scanner,
Thulborn has mapped a two-stage recovery process in patients who
lost their language skills after strokes. In one patient suffering
from damage to Wernicke's area (the region in the left cortex that
controls the understanding of language), functional MRI showed that
the brain initially recouped by allocating speech comprehension to
an area on the opposite side of the brain. Over time, while
Wernicke's area remained damaged, an adjacent area took on this
cognitive task.
The ability of the brain to maintain performance by recruiting
undamaged portions of the cortex may suggest why functional recovery
can occur even after large strokes. One key factor in recovery time,
Thulborn suggested, is whether white matter has been damaged. White
matter consists of myelinated neuronal axons that serve as cables
linking the different areas of the cortex. When these are injured,
vital connections needed to allocate functions elsewhere are lost.
The involvement of white matter tracts portends slower and reduced
recovery. This may reflect reduced capacity to redistribute workload
when the connectivity through white matter is disrupted.
While functional MRI has been largely used in research to map
brain functions, it is just beginning to find clinical applications.
At the UIC Medical Center, Thulborn is collaborating with other
physicians, psychologists and therapists to use the technology in
designing and monitoring rehabilitation programs aimed at restoring
lost cognitive and motor skills. In this role, Thulborn said,
functional MRI can guide and refine therapies to enhance the brain's
innate plasticity. The very-high-field MRI scanner works by picking
up faint magnetic signals in the underlying tissue. As neurons
become increasingly active in specific regions of the brain, blood
flow surges to those regions and blood volume expands.
In the process, deoxygenated blood is replaced with oxygenated
blood, the two differing in their magnetic properties. The MRI
scanner is able to detect this magnetic change, although minute,
because of the scanner's high magnetic field strength: 3.0 Tesla,
twice that of MRI scanners more commonly deployed in clinical
settings. (A Tesla is equivalent to 10,000 gauss; the magnetic field
strength of Earth is less than one gauss.) Cross-sectional images
are made through the entire brain to create a three-dimensional
view. The images must be run through a series of statistical
programs so that they can be correctly interpreted.
To obtain images of the working brain, patients are placed on a
table and moved into the center of the magnet. The images are taken
while patients are engaged in a set of cognitive tasks devised to
correlate functional activities with specific areas of the brain. To
map the language comprehension network of the brain, for example,
patients are given sentences of varying complexity to read and asked
to answer true/false questions by pressing a finger switch. To map
the motor and sensory areas, patients simply tap a finger.
References:
Blumer, D., & Benson, D. Personality changes with frontal and
temporal lesions. In D.F. Benson and F. Blumer, eds. Psychiatric
Aspects of Neurologic Disease. New York: Grune & Stratton, 1975.
Blumer, D., & Walker, E. The neural basis of sexual behavior. In
D.F. Benson and F. Blumer, eds. Psychiatric Aspects of Neurologic
Disease. New York: Grune & Stratton, 1975.
Carlson, Neil R. Physiology of Behavior sixth edition. Allyn and
Bacon (1988) Massachusetts.
Kolb, B., & Whishaw, I. (1990). Fundamentals of Human
Neuropsychology. W.H. Freeman and Co., New York.
Milner, B. (1968). Visual recognition and recall after right
temporal lobe excision in man. Neuropsychologia, 6:191-209.
Milner, B. (1975). Psychological aspects of focal epilepsy and its
neurosurgical management. Advances in Neurology, 8:299-321.
Read, D. (1981). Solving deductive-reasoning problems after
unilateral temporal lobectomy. Brain and Language, 12:116-127.
Taylor, L. (1969). Localization of cerebral lesions by psychological
testing. Clinical Neurosurgery, 16:269-287.
Anne Serene
Effects of a brain lesion to Wernicke's Area/Temporal Lobe from the
spouses and Family Members Point of View
The approach taken by family members after an injury differs
from that of a professional. Family members typically need an
fundamental understanding of what causes an injury, what the effects
of the injury sustained by a love one is and how best to deal with
it to help their loved one.
Any injury or mishap can be difficult for the spouse and
family of the person involved. This is even more so when brain
functions are affected. This is common when someone has suffered a
stroke, sometimes referred to as a cerebrovascular accident. This
most commonly occurs when a blood vessel is blocked depriving the
area of the blood supply. The result is that cells die. One of the
regions that can be affected is Wernicke's Area in the temporal
lobe.
Wernicke's Area is named for Carl Wernicke who first described
it in 1874. Werenicke's area is located in the left temporal lobe
and appears to be crucial for language comprehension. People who
have suffered damage from this area from a stroke or other means
suffer from Wernicke's Aphasia, sometimes called fluent aphasia.
Wernicke's Aphasia is difficulty comprehending and producing
language do to damage to this area. People with Wernicke's Aphasia
are unable to understand the content words while listening, and
unable to produce meaningful sentences; their speech has grammatical
structure but no meaning. Their speech patterns and behaviors
appear normal, but phrases are jumbled and the words that would
normally bring content to what they are saying are missing.
Normally, when listening, auditory and speech information is sent
from the auditory area to Wernicke's area for analysis of the words
that normally convey content, then to Broca's area for analysis of
syntax. When speaking, content words are selected by Wernicke's
area, grammatica1 refinements are added by Broca's area, and then
the information is sent to the motor cortex, which sets up the
muscle movements for speaking. (Gray, 1994; Reber, 1995)
A loved one with Wernicke's aphasia can perform most of the
same activities they could before. It is their understanding of
speech content and their ability to create speech content that is
impaired. Linguistically they still convey emotion. They still
follow the protocols that we normally follow when carrying on a
conversation.
Wernicke's Aphasia effects language in three ways. Fluent
Aphasia affects the ability to comprehend the meaning of words.
Depending on the severity of the aphasia a loved one will not
understand the meaning of words, although in cases with less damage
they do retain the ability to comprehend a limited number of words.
It also affects, the ability to convert thoughts to words. While a
loved one will be able to maintain a dialog, their sentences will
containing few contents words and many connective phrases structured
such a way that won't make sense This effects the ability to
produce speech with content or meaning. Wernicke's Aphasia does
not seem to impair their ability to derive meaning from vocal tone
or facial expression.
Even though they lack the ability to understand or create
language content maintaining verbal interaction seems to be
beneficial. Also, the brain seems to maintain a degree of neural
plasticity even into later life. Research seems to indicate that
some of the functions of Wernicke's area may be transferred to the
corresponding portion of the right temporal lobe (Centre for Neuro
Skills, 1999). Maintaining interaction seems to be essential to
this process. A content directed reduced speech form might also be
helpful in restoring some content processing.
Although research data is limited, there have been cases where
sign language has been effectively used to a limited degree in cases
of Wernicke's Aphasia (Kirk, 2001). The corresponding side and
often temporal region in some cases is involved in processing the
spatially based American Sign Language (Hickok et al., 1998). In
some patients Wernicke's Aphasia has brought on it's own impairment
to the use of American Sign Language (Hickok et al, 1999). The use
of American Sign Language is being examined as a means for those
with Wernicke's Aphasia to communicate with some success (Kirk,
2001). It appears that portions of the left occipital lobe as well
as portions of the left temporal lobe are involved in processing
American Sign Language (Hickok et al, 1996). The result is a
greater ability to communicate through some forms of sign language
than is possible by speech seems to be possible in those with damage
to their right temporal lobe (Kirk, 2001), although the ability to
communicate with sign language is also impaired (Hickok, 1998). Up
to this point sign language use was examined as a way to restore
communication in those already fluent in it's use. It was found
useful in those that natively learned and in some individuals that
had learned pure dialects of American Sign Language. It did not
seem effective in those that used intermediate forms (usually used
by those that learn sign language as an adult) that retain many
elements of spoken English. There has been some success in the use
of sign language in those that had intermediate forms or no
knowledge in American Sign Language.
For the loved one's of those suffering from Wernicke's Aphasia
there is no definite answers on the best course of action. The
research shows that maintaining interaction is important and that
sign language has been useful in some cases, although there are
still many unanswered questions as to many of the factors involved.
REFERENCES
Centre for Neuro Skills, 1999. "Brain Compensates for Damage to
Language Systems" Inside View: A Quarterly Newsletter Dedicated to
Traumatic Brain Injury Issues. #8(3), p. 6.
Gray, Peter. (1994). Psychology. New York, NY: Worth Publishing.
Hickok, Gregory; Wilson, Margaret; Clark, Kevin; Klima, Edward S.;
Kritchevsky, Mark; and Bellugi, Ursula. 1999. "Discourse Deficits
Following Right Hemisphere damage in Deaf Signers." Brain and
Language. Vol 66(2): 233-248.
Hickok, Gregory; Kirk, Katherine; and Bellugi, Ursula. 1998.
"Hemispheric Organization of Local- and Global-level Visuospatial
Processes in Deaf Signers and its Relation to Sign Language
Aphasia." Brain and Language. Vol 65(2): 276-286.
Hickok, Gregory; Bellugi, Ursula; and Klima, Edward S. 1996. "The
Neurobiology of Sign Language and Its Implications For the Neural
Basis of Language." Nature. Vol 381(6584): 699-702.
Kirk, Sharon. 2001. "Sign Language Program Restore Communications
After a Stroke." Gallaudet Today. 65(1): 9.
Reber, Arthur S. 1995. The Penguin Dictionary of Psychology. New
York: Penguin Books.
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