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Neurological Basis of Behavior (PSY - 610)

Lesson43

Higher Order Brain functions

Objectives:

The students would be familiarized with the role of higher order brain functioning in disorders of

speech, motor and sensory apraxias, memory and amnesias.

Brain correlates

a) Language Speech Production Comprehensions, Aphasias

b) Visuospatial, The man who mistook his wife for a hat?

c) Apraxias. (Neuropsychological tools)

d) Brain correlates of Learning and Memory, Amnesia, Verbal, Non verbal memory,

e) (Neuropsychological tools)

Aphasia and Dyslexia:

Aphasias and Dyslexia are related because the spoken words are transferred to written language.

Reading and writing is closely tied to listening and speaking auditory modality). Wernicke's aphasia is

accompanied by dyslexia.

Interestingly, there are more dyslexics with Wernicke's aphasia in English and other western language,

but not so in Chinese where each word is represented individually or where the sign language (spatial

not auditory modality) is used.

Chinese aphasics retain ability to write accurately. The Japanese language comprises of two forms the

Kanji and the Kana. The Kanji symbols are the pictographs adopted from the Chinese language. These

are the visual representation of concepts, thus a house would be shape of a Pagoda. On the other hand

the Kana symbols are acousitic or Phonetic representations. Thus Kana (sound, auditory mode), and

kanji (visual mode) Sasanuma (1975) reported that left temporal lobe lesions affected the writing of the

Kana symbols but not the Kanji where visual cortex is involved).

The Japanese language: 3 phonetics and 1 pictograph

Mode:

Kana

Kanji

Brain areas

left temporal lobe

Visual cortex

Generally most languages use sound and acoustic signals and cues to write (look at how recite our

nursery rhymes and how we remember the correct spelling of words). The question is if we are so

dependent on the sound for language what about the deaf? Interestingly the deaf are not dyslexics with

receptive aphasia (as they read without phonetics (Braille, the language script of the blind is a touch

language)

Aphasias related to speech

A wide range of disorders even within the major aphasias, the characteristics differ with areas of

damage. We will disucss some of this aphasia in brief.

a) Conduction Aphasia: is produced when damage to inferior parietal zone disconnects the axonal

fibres connecting the Brocas and the Wernicke's areas. Conduction aphasics have meaningful,

paraphrasic speech, somewhat fair comprehension, but poor repetition (they can repeat single and

meaningful words, but not non-meaningful words)

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Neurological Basis of Behavior (PSY - 610)

b) Anomic Aphasia: This is aphasia specific to names. They have difficulty in finding the right word,

so they use circumlocution going the round about way

I had a patient who had anomia after a stroke

When asked to identify a stapler in a picture: What is it?

He replied, it is used in the office.

Yes, but what is it?

It is used to pin papers together

Yes, but what is it?

He showed how it worked

Yes but what is its name

He could not give the name even after several attempts.

This illustrates that he knew what it was, what it was used for, but could not name it.

There are cortical aphasias and Trans cortical aphasia, and sub cortical aphasias, but we would not be

discussing the whole classification, this should be enough to give you an idea.

Dyslexia: (Reading, Writing, Mathematics)

Reading and writing disorders are related to the kind of aphasia that patients have. The patient with

Wernicke's aphasia would have difficulty reading and writing as they do comprehending speech.

Broca's aphasics have difficulty in reading out aloud; their writing and speech both are agrammatical

a) Alexia with Agraphia:

This is a difficulty in which the person has difficulty in reading and writing. This is caused by damage

to the left angular gyrus in the parietal lobe (angular gyrus is at the borderline of visual, auditory and

somatosensory cortices therefore it may affect skills involving all three modalities

b) Pure Alexia:

This is actually word blindness, where alexia occurs without agraphia: patient can write but cannot read

what he writes. Although they cannot read, they can recognize the words if they are spelled out to them.

Pure Alexia is a perceptual disorder, similar to pure word deafness only it is visual not auditory.

c) Agnosias are disorders related to sensory modalities either auditory or visual

Disorders of auditory perception Agnosias:

An auditory agnosia is the impaired capacity to recognize auditory stimuli, perhaps due to a disturbance

of perceptual processes more than sensations. There appears no problem with the input of information

but of giving it meaning and of recognizing it.

We will discuss only two of these here

a) Amusia

b) Agnosia for Sounds

1. Amusia: subdivisions of this disorder are tone deafness: inability to discriminate various tones of

musical scales, and Music deafness: impaired recall or recognition of a melody, tune) as well as rhythm,

measure, or tempo (beat), and Receptive amusia; difficulty in discriminating basic notes of music or

series of notes of pitch, rhythm etc

2. Agnosia for sounds: inability to identify what the different nonverbal sounds mean (classification

difficulty? For example if there are different kinds of bells ringing --church, school, telephone, the

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Neurological Basis of Behavior (PSY - 610)

patient cannot tell the difference. These sounds may sound all alike, or may be confused for each other.

So basically it's discrimination and categorization deficit.

For these disorders it appears that the bilateral temporal regions are involved

Visual deficits: These are deficits related to integration or processing of visual information. Agnosia is

a failure of recognition, not due to sensory (the input is all right) or intellectual problems (the patient

does not have any intellectual impairment).

Visual Agnosia: is Agnosia for visual stimulus. It is not a seeing deficit, as the patient can see but

cannot put the pieces of visual input together in a coherent form.

Very interesting deficit: Prosopagnosia

Prosopagnosia is Visual Agnosia: Faces is the first key you have to other people- friend or foe? There

is a dictionary of features of faces where every face is immediately matched. Prosopagnosics have

difficulty recognizing a face know it is a face but who?

The patients report seeing parts such as nose, eyes, lips but cannot put it together. In order to recognize a

face you have to match and put together the entire feature in a coherent face. In extreme form of this

deficit patients cannot even recognize themselves in the mirror. This is due to damage to the

Inferotemporal region. There are some patients who have difficulty recognizing only the familiar faces,

while others have difficulty in recognizing unfamiliar faces. They can sometimes use a cue such as a

mole or a scar to recognize a face. It is a visual-limbic disconnection (especially for familiar faces) of

the Right hemisphere region

Apraxia is movement or motor difficulties when required to perform at a verbal command. Though

these tasks can be performed spontaneously (can be copied) without problems. Apraxias are bilateral but

usually produced by the left hemisphere lesion. This deficit was first described by Hughlings-Jackson

Apraxia: Greek word praxis: no action. The missing or inappropriate action is not due to paralysis or

difficulties of motor movement, or of understanding of instructions, or motivation, but difficulty in

carrying out the action required.

Construction Apraxia: is tested by asking the patient to copy or draw or build blocks in a given design.

There is both left hemisphere and right hemisphere damage. LH is oversimplification, very little details,

whereas RH damage leads to loss of overall gestalt

We have seen some of the deficits which are caused by damage to the cortical areas. This requires

complex neuropsychological examination and rehabilitation strategies can be developed keeping each

patients individual deficits in mind

References:

1. Carlson N.R. (2005) Foundations of Physiological Psychology Allyn and Bacon, Boston

2. Pinel, John P.J. (2003) Biopsychology (5th edition) Allyn and Bacon Singapore

3. Bloom F, Nelson and Lazerson (2001), Behavioral Neuroscience: Brain, Mind and Behaviors (3rd

edition) Worth Publishers New York

4. Bridgeman, B (1988) The Biology of Behaviour and Mind. John Wiley and Sons New York

5. Brown,T.S. and Wallace.(1980) P.M Physiological Psychology. Academic Press New York.

6. Bradshaw J.L. and Mattingley, J.B. (1995) Clinical Neuropsychology: Behavioral and Brain

Sciences. ACADEMIC PRESS

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