A COMPARATIVE STUDY OF THE MIDDLE LATENCY AND

P300 RESPONSES OF THE AUDITORY EVOKED POTENTIALS

IN THE TOTALLY BLIND AND NORMAL SUBJECTS

By

Dr.Manjula.P
Dissertation Submitted to the
Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment
of the requirements for the degree of

DOCTOR OF MEDICINE

In

PHYSIOLOGY

Under the guidance of

Dr. Roopakala. M.S
Department of Physiology

M.S. Ramaiah Medical College

Bangalore

2011
 DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled “A Comparative Study of the Middle
latency and P300 responses of the Auditory Evoked Potentials in the Totally Blind and
Normal Subjects” is a bonafide and genuine research work carried out by me under the
guidance of Dr. Roopakala M S.,Professor, Department of Physiology, M S Ramaiah Medical
College,Bangalore.54.

Signature of the Candidate

Name Dr.Manjula.P

Date:

Place: Bangalore.54

.
 CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled “A Comparative Study of the Middle

latency and P300 responses of the Auditory Evoked Potentials in the Totally Blind and

Normal Subjects “is a bonafide research work done by Dr.Manjula.P in partial fulfillment of

the requirement for the degree of M.D in PHYSIOLOGY.

Signature of the Guide

Name: Dr. Roopakala M S

Designation & Department: Professor

Department of Physiology
M S Ramaiah Medical College

Date:

Place: Bangalore.54
 ENDORSEMENT BY THE HOD

This is to certify that the dissertation entitled “A Comparative Study of the Middle

latency and P300 responses of the Auditory Evoked Potentials in the Totally Blind and

Normal Subjects” is a bonafide research work done by Dr.Manjula.P in partial fulfillment of

the requirement for the degree of M.D in PHYSIOLOGY under the guidance of Dr. Roopakala

M S., Professor, Department of Physiology, M S Ramaiah Medical College, Bangalore.54.

Signature of the HOD

Name: Dr.Jaisri.G

Date:

Place: Bangalore.54.
 ENDORSEMENT BY THE PRINCIPAL

This is to certify that the dissertation entitled “A Comparative Study of the Middle

latency and P300 responses of the Auditory Evoked Potentials in the Totally Blind and

Normal Subjects “is a bonafide research work done by Dr.Manjula.P in partial fulfillment of

the requirement for the degree of M.D in PHYSIOLOGY under the guidance of Dr. Roopakala

M S., Professor, Department of Physiology, M S Ramaiah Medical College, Bangalore.54.

Seal & Signature of the Principal

Name:

Date:

Place: Bangalore.54.
 COPYRIGHT DECLARATION BY THE CANDIDATE

I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall

have the rights to preserve, use and disseminate this dissertation in print or electronic format for

academic / research purpose.

Signature of the Candidate

Name: Dr.Manjula.P

Date:

Place: Bangalore.54.
 ACKNOWLEDGEMENT

The completion of this dissertation was possible with the guidance, assistance and

encouragement given in this regard to me by a number of people.

First of all, I deem it my proud privilege to have the opportunity to work with my Guide

Dr.Roopakala M S, Professor, Dept of Physiology M. S. Ramaiah Medical College, Bangalore.

Her constant suggestions, encouragement and timely advices have been invaluable in this work

of mine.

I am thankful to my Co-Guide, Dr.Srinivasa R, Professor and Head of the Department,

Neurology, M.S. Ramaiah Teaching Hospital, Bangalore for his excellent clinical acumen and

guidance which instilled in me the necessary skills to understand the intricacies of this work.

I am very thankful to Dr.Jaisri G, Professor and Head of the Department, Physiology, M.

S Ramaiah Medical College, Bangalore for her ever encouraging support, advices and the

genuine concern towards my work.

I sincerely thank the administration and Principal Dr.Kumar, M. S Ramaiah Medical

College, Bangalore for providing me with all the adequate facilities for the completion of the

work and my studies.

I sincerely thank the Indian Council of Medical Research, New Delhi for recognizing my

work and giving me an award.

I sincerely thank the faculty of the Department of Ophthalmology, M. S. Ramaiah

Medical Collage, Bangalore for their services towards the ophthalmologic screening of the blind

and normal subjects.

I sincerely thank Mr.Swamy for teaching me the method of the AEP recordings.
 I sincerely appreciate Mr. Suresh K. P, scientist (Statistics), National Institute of Animal

Nutrition and Physiology, Bangalore for the statistical analysis of the acquired data.

I sincerely thank Dr.Venkatesh D, Dr.Vasanthi Ananthakrishnan, Dr.Tara Christopher,

Dr.Preethi B L, Dr. Ambarish V, Dr.Dayananda G, Dr.Vijayadas, Dr.Kirthana K, the teaching

staff and all the postgraduates of the Department of Physiology for their suggestions and timely

advices.

I sincerely thank Jeeva Jyothi, School for the Blind, Bangalore for their cooperation in

organizing the blind subjects for the study.

The work ofcourse would not have progressed without the cooperation of the Blind and

Normal individuals who need a special mention of thanks.

I would like to thank my family for their immeasurable support and tolerance.

Most of all I sincerely thank the Almighty God who blessed me with the wisdom and

strength to accomplish this work.

Signature of the Candidate

Name: Dr.Manjula.P

Date:

Place: Bangalore.54.
LIST OF ABBREVIATIONS USED

AEP: Auditory Evoked Potential

Ag/AgCl: Silver/ Silver Chloride

Ann Neurol: Annals of Neurology

Arq Neuropsiquiatr: Arquivos de Neuropsiquiatria

Brain Res: Brain Research

Br J Psychol: British Journal of Psychology

Cogn Brain Res: Cognitive Brain Research

dB: Decibel

EB: Early Blind

ERP: Event Related Potential

Eur. J. Neurosci: European Journal of Neuroscience

fMRI: Functional Magnetic Resonance Imaging

Int J Neurosci: International Journal of Neurosciences

J Neurophysiol: Journal of Neurophysiology

J Neurosci: Journal of Neuroscience

LLAEP: Long Latency Auditory Evoked Potential

LMP: Last Menstrual Period

MLAEP: Middle Latency Auditory Evoked Potential

OPD: Outpatient Department

PN: Processing Negativity

TMS: Transcranial Magnetic Stimulation

V I: Visual Cortex
 ABSTRACT

Background and objective:

The totally blind individuals are often considered to be compensated for their visual loss

by augmentation in the auditory and tactile perceptions as compared to the sighted individuals.

The objective of the present work was to compare the MLAEP and P300 components of the

auditory evoked potentials in the totally blind and the normal sighted individuals.

Methods:

MLAEP and P300 were recorded in 20 totally blind females and compared with 20 age

matched normal sighted females. Mean latency and amplitude of the waveforms Na, Pa and Nb

of MLAEP and P300 were measured and analyzed statistically using Student t test (two tailed,

independent).

Results:

The mean latencies of all the waveforms were significantly reduced in the blind subjects

compared to the normal subjects (p‹0.001). The mean amplitudes of the waveforms Na, Pa and

Nb did not show any significant changes between the two groups. The mean amplitude of the

waveform P300 at Oz site was significantly increased in the totally blind (p‹0.05).

Conclusion:

This study suggests that the totally blind individuals demonstrate remarkably reduced

latency suggesting increased conduction velocities and thus a much better information

processing in the auditory system. The increase in amplitude at the Oz site for P300 recording
suggests that the visual cortex also participates in hearing in the totally blind compared to the

normally sighted individuals which indicates cross-modal plasticity.

Keywords:

Totally blind, normal sighted, auditory evoked potentials, MLAEP, P300, cross- modal

plasticity.
 TABLE OF CONTENTS

1. Introduction Page No.1-3

2. Objectives Page No.4

3. Review of Literature Page No.5-20

4. Methodology Page No.21-28

5. Results Page No.29-39

6. Discussion Page No.40-44

7. Conclusion Page No.45

8. Summary Page No.46

9. Bibliography Page No.47-56

10. Annexures Page No.57-62

 LIST OF TABLES

Sl.No Tables Pages

1 Comparison of age distribution of subjects 31

Comparison of Age, Height and Weight and Head circumference of

2 32
subjects

3 Comparison of Number of days from LMP between the two groups 35

4 Comparison of MLAEP LATENCY between the two groups 36

5 Comparison of MLAEP AMPLITUDE between the two groups 37

6 Comparison of P300 (amplitude and Latency) between two groups 38

 LIST OF FIGURES

Sl.No Figures pages

Comparison of age distribution of subjects between the two groups

1 31

2 Comparison of Age of subjects between the two groups 32

3 Comparison of height of subjects between the two groups 33

4 Comparison of weight of subjects between the two groups 33

5 Comparison of Head circumference between the two groups 34

Comparison of Number of days from LMP between the two groups

6 35

7 Comparison of MLAEP LATENCY between the two groups 36

8 Comparison of MLAEP AMPLITUDE between the two groups 37

9 Comparison of P300 amplitude between two groups 39

10 Comparison of P300 latency between two groups 39

 INTRODUCTION

The blinds are often compensated for their handicap by developing supranormal abilities

in their remaining sensory systems like the auditory and the somatosensory systems.

Studies done in specific electrophysiological recordings have reported plasticity changes

in the involved neural tracts and the higher central nervous system in the totally blind in

response to blindness and that they depend on the nonvisual sensory modalities1, 2,3,4,5.

Neuro plasticity is an important adaptation. It is the capacity of the nervous system to

modify its organization by the changing of neurons, their networks and their function by new

experiences. Such changes can occur as a consequence of many events, including the normal

development and maturation of the organism, the acquisition of new skills (learning) 6.

These changes are beneficial and the brain continually responds to changes in stimuli by

reorganizing itself. Brain reorganization occurs every day to promote learning.

During the 20th century, the consensus was that the neocortical areas of the brain could

not change in structure after childhood unlike the hippocampus and dentate gyrus, where new

neurons continue to be produced into adulthood.

This belief is challenged by new findings suggesting that all areas of the brain are

plastic even after childhood. This is an evolutionary mechanism that allows people with the

deprivation of a sense to adapt and compensate.

1
 Sensitive/Critical period is the developmental time period during which experience can

significantly alter the organisms’ behavioral performance and related aspects of the brain

structure and/or function.

Cross -modal plasticity refers to the capacity of the brain to replace the functions of a lost

part by another part. This cross modal plasticity has been documented both in animals and

humans deprived of a particular sensory modality such as vision or audition. The most

commonly used form of sensory substitution is Braille reading, which enables the blind to read

by using the somatosensory system7, 8, 9.

Studies have shown augmentation of the auditory evoked potentials in the totally blind in

comparison with the normally sighted2, 3, 4, 5

. It has been reported that the components of the

middle latency auditory evoked potentials (MLAEP) have shorter latencies in the blind compared

to normally sighted 10.

But not much has been documented on the P300 response of the long latency component

of the auditory evoked potential (LLAEP) in the blind. Thereby, the present work is undertaken

to advance our understanding of MLAEP and P300 responses in the blind and the probable

plasticity of the auditory system in response to blindness.

Auditory evoked potentials (AEPs) are a subclass of Event related potentials (ERPs). For

AEPs, the "event" is a sound. AEPs are the electrical potentials generated by the nervous system

in response to brief sound stimulation. AEPs are classified into early (the first 10 to 15

milliseconds), middle (10 to 80 ms) and late (80 to 750 ms) components.

The recording of AEP is a noninvasive technique, which allows the selective

investigation of the auditory pathways. Their amplitudes are very small and they are elicited after

stimulus presentation at different latencies. They can be extracted from the temporally random

2
background activity by making several successive recordings and averaging all the data acquired

after each stimulus. Resulting waveforms show voltage as a function of time. The components

are labeled according to their sequence by polarity. The latency and amplitude of the components

are measured. The latency studies the conduction velocity of nerve impulses; the amplitude

studies the number of nerve cells which are stimulated.

Hypothesis:

“When vision is completely lost, there is augmentation and much better information

processing in the auditory systems compared to the normally sighted individuals”.

3
 OBJECTIVES

1) To compare the peak latencies of Pa, Na and Nb waves of MLAEP in the totally blind and

normal sighted subjects.

2) To compare the peak latency and the amplitude of P300 wave in the totally blind and normal

sighted subjects.

4
 REVIEW OF LITERATURE

AUDITORY PATHWAY REVIEW

The afferent fibers in the auditory division of the eighth cranial nerve end in dorsal and

ventral cochlear nuclei. From there, auditory impulses pass by various routes to the inferior

colliculi, the centers for auditory reflexes, and via the medial geniculate body in the thalamus to

the auditory cortex. Other impulses enter the reticular formation. Information from both ears

converges on each superior olive, and beyond this, most of the neurons respond to inputs from

both sides. The primary auditory cortex is Brodmann's area 41.

In the primary auditory cortex, most neurons respond to inputs from both ears, but

strips of cells are stimulated by input from the contralateral ear and inhibited by input from the

ipsilateral ear. There are several additional auditory receiving areas, just as there are several

receiving areas for cutaneous sensation; the auditory association areas adjacent to the primary

auditory receiving areas are widespread. The olivocochlear bundle is a prominent bundle of

efferent fibers in each auditory nerve that arises from both ipsilateral and contralateral superior

olivary complexes and ends primarily around the bases of the outer hair cells of the organ of

Corti.

5
A

AUDITORY PATHWAY

Primary Auditory Cortex

Impulses ascend from the dorsal and ventral cochlear nuclei through complex paths that

are both crossed and uncrossed. In experimental animals, an organized pattern of tonal

localization occurs in the primary auditory cortex (area 41), as if the cochlea had been unrolled

on it. In humans, low tones are represented anterolaterally and high tones posteromedially in the

auditory cortex. This pattern normally develops in early life, and its development is slowed if the

6
animals are exposed to a constant low level of noise. If the noise is then stopped, development

resumes at its normal rate11.

AUDITORY EVOKED POTENTIAL (AEP)

Auditory evoked potentials components

The Auditory Evoked Potential (AEP) is an electrical manifestation of the brain’s

response to a physiological or an electrical (preferred as it can be easily controlled, measured and

produces potentials of great amplitude) auditory stimulus.

7
 They provide an objective measure of the function in the auditory system. They yield

reproducible results and are reliable diagnostic tests. AEPs are recorded using commercially

assembled equipment that follows essential standards. Galileo NT is one such instrument.

AEP waveforms are labeled according to their polarity and peak latency.

The middle latency auditory response (MLR) is a synchronic auditory evoked potential

that occurs in a time space of approximately 10-80 milliseconds (ms) after the auditory

stimulation composed by a series of positive and negative waves. The first MLR wave is the Na

(occurring at around 18 ms) followed by the Pa (30 ms), Nb (40 ms), Pb (50 ms) and sometimes,

Nc and Pc; the Pa wave has the greatest amplitude, and is more consistent and more frequently

used .

The MLR has multiple generators reflecting primary and non-primary areas, such as the

reticular formation, the thalamus divisions; with a greater contribution of the thalamo-cortical

pathways and with a lesser contribution of the inferior colliculi (mesencephalus) and auditory

cortex12.

The late latency potentials are less affected by the physical properties of the stimulus and

are more affected by the functional use that the individual makes of the stimulus, being less

determined by the frequency or intensity, and more by the attention to the sound stimulus. Such

potentials are useful in the cognitive and attention functions study.

The P300, also called cognitive potential, is a positive late latency auditory evoked

potential generated by a series of stimuli (frequent) and by the occasional occurrence of a less

frequent stimulus (rare) that appears randomly. The rare stimulus occurs from 15 to 20% of the

total stimuli, and the subject should identify it counting mentally or pressing a button every time

it occurs. At each screening, two waves are recorded; one for the frequent stimulus and one for

8
the rare stimulus. The auditory system habituates to hearing the frequent stimulus and, therefore

less neurons answer to this stimulus. Concerning the rare stimulus, as it is heard less times, the

system answers to this stimulus with more neurons generating a wave with greater amplitude.

The P300 wave is the greatest positive wave after the complex N1-P2 occurring between

240 and 700 ms.

A latency increase or an amplitude decrease indicates clinical and sub-clinical problems.

13
According to Picton , if the P300 is small or late, there will probably be a deficit in the

cognitive processing. The latency is a more reliable indicator than the amplitude.

The exact generator of P300 is still not known. Different areas of the brain such as

inferior parietal lobe, frontal lobe, hippocampus, medial temporal lobe, insula and other limbic

structures have been reported to contribute to scalp recorded P30014 .

Peak latencies of cortical AEPs increases and the amplitude decreases with advancing age
14
.

AEP latencies in normal, healthy, young ovulating women showed a decrease during

progesterone phase when compared with those from estrogen phase. There was no significant

difference between the estrogen and the ovulatory phase AEPs. AEPs showed no changes in their

amplitudes in all phases of menstrual cycle15.

NEUROPLASTICITY

Object perception benefits from the coordinated interplay of vision, audition and touch.

These different sensory modalities work together to provide full information about an object 16.

Single sensory modality deprivation provides a unique opportunity to investigate plastic changes

in brain function.

9
 Brain plasticity is the brain’s ability to adapt to the complete absence or the deterioration

of a sense. Sensory substitution is therefore most likely explained through the study of brain

plasticity. Cortical re-mapping or reorganization takes place when the brain experiences some

sort of deterioration. This is an evolutionary mechanism that allows people with the deprivation

of a sense to adapt and compensate by using other senses17.

Plasticity involves changes in the cortical representation of the analyzed area due to an

enhanced peripheral input secondary to an adaptive phenomenon of cortical representation18.

Plastic changes that take place in the central nervous system and neuronal networks are

part of the structural and physiological substrate for recovery of function after injury 19.

There is an intimate relationship between learning, behavior and memory with brain

functions20.

The cortical reorganization of the primary somatosensory representational areas in adult

monkeys occurs after an increased sensory input to a particular portion of the brain21. On the

contrary, such reorganization also occurs due to a decreased sensory input produced by

deafferentation22.

It has been shown by combined magnetic and potential recordings that the cortical

sensorimotor representations are substantially reorganized in adult rats after peripheral motor

nerve transection23. Cortical mapping has shown that somatosensory cortex representation

reorganizes after dorsal root damage/denervation of the paw in adult cats 24, 25or after amputation

of digits in adult monkeys 26.

The facial vibrissae show supernormal growth in both cats and mice that have been

deprived of vision from birth. Further, the whisker representation in the somatosensory cortical

barrel field shows a concomitant enlargement in binocularly enucleated mice: individual barrels

10
are expanded in size by up to one-third. The increased use of the vibrissae in visually deprived

animals may stimulate both their own growth and, via activation of the respective neural

pathways, the expansion of their central representation 27.

The vibrissal representational area in adult rats reorganizes after vibrissa trimming,

resulting in heavy differential stimulation of a limited subset of vibrissae28.

Brain mapping of the preferred hand in adult monkeys shows a more elaborate

sensorimotor cortical representational area than that of the non-preferred hand which suggests

that use-dependent preference of the hand has a role in its cortical representation29.

Other studies also indicated that when attention is directed to peripheral auditory space,

there is enhanced speech recognition and mapping of the auditory cortex in the congenitally

blind than in normal sighted people2.

Changes encountered in the auditory cortex of blind individuals are as a consequence of

the absence of visual input in combination with enhanced auditory activity generated by the long-

term concentration by blind individuals on non-visual cues to interact appropriately with the

environment. An expansion of regions within the auditory cortex was expected as an indication

of use-dependent cortical reorganization. This suggests that blind individuals have better auditory

spatial ability than individuals with visual cues; therefore, some perceptual compensation

occurred in the former5.

Differences in the scalp distribution of brain electrical activity between the normal

sighted and the totally blind suggest a compensatory reorganization of brain areas in the blind

that may contribute to the improved spatial resolution for acoustic sources in peripheral auditory

fields and to decode speech 3.

11
 Increased reliance on the auditory modality would give rise to alterations in the auditory

areas of the brain and its perception abilities. Experimental evidence has indicated an increased

prevalence of absolute pitch in blind musicians4.

Congenitally blind subjects were reported by Strelow and Brabyn to show sensitivity in

auditory perception, enabling them to use echoes to perceive spatial positions of objects30.

Early blind individuals also show selective attention enhancements that may contribute to

better auditory perceptual skills. The widespread preparatory activity in the EB subjects within

auditory cortical areas may reflect biasing effects that could contribute to their superiority in a

range of auditory perceptual and cognitive abilities3.

Thus, there is a compensatory adaptation of the auditory system in the congenitally blind,

presumably because of a reorganization of the neocortex.

Study in individuals who were deprived of other sensory modalities has also shown

similar changes. The congenitally deaf humans are faster and more accurate than normal hearing

subjects in detecting visual peripheral movements 31 and also have superior tactile sensitivity 32.

Brain reorganizes itself in response to blindness, possibly as a result of the blind

individuals’ greater attention to and reliance on nonvisual sensory avenues to maintain adequate

relation with the world around them. The expansion of the tonotopic map, the reorganization of

the somatosensory cortex and the cross-modal plasticity in the blind would appear to be an

excellent composite example of the continual competition for cortical space33.

When there is increased use of a body part for sensory discrimination, the

representational zones within the brain normally responsible for mediating those functions

expand at the expense of other regions that are currently not being used to the same extent 3.

12
 Whether or not the full range of perceptual ability is improved in the blind, it is

nevertheless the case that sensory input from nonvisual avenues becomes of greater behavioral

relevance to these individuals to enable effective interaction with the world around them.

Focused attention on behaviorally relevant stimulation over extended periods has been found to

produce a substantial enlargement in the representational zones of the involved portions of the

body in somatosensory cortex in research with animals18, 33 and humans34, 35 .

Training which is use dependent and aimed at acquiring skills, can result in distortions of

the body surface and movement representations in the cortical representational map zones and in

turn lead to behavioral gains towards better performance 36 .

The mature mammalian nervous system alters its functional organization in a use-

dependent manner. Enhanced stimulation of a body part enlarges its cortical representational

zones and may change its topographic order. The motor cortical representation of a body part

expands with increased activity of that particular part37.

The number of neural circuits in the right primary motor cortex devoted to the left hand

cannot be known in advance of an individual making a special demand for left hand skills such

as required for piano playing. However, due to neural plasticity, neural circuits can assign

themselves: as a result the brain area dealing with the left hand is larger in pianists than in

nonpianists, an expansion that directly correlates with increased left hand dexterity. The

plasticity probably resulted from short-term strengthening of specific connections between

neurons, rather than from sprouting of new connections38.

New techniques or a modification of existing techniques might be able to induce more

lasting effects on the reorganization. Techniques like long-term Transcranial Magnetic

13
Stimulation (TMS) or drug therapy, combined with practice or physical therapy, may be able to

change brain circuitry as well as strengthen connections39.

Many other studies have shown that the brain continually responds to changes in stimuli

by reorganizing itself. These changes are often beneficial. For example, people who have been

blind from an early age often use part of the brain region normally employed for vision to

process auditory sensations, which helps them in localization of peripheral sound and speech

detection. However, in other cases, brain reorganization may lead to problems such as phantom

limb pain40. The neural mechanisms underlying this plasticity changes remain elusive.

CROSS-MODAL PLASTICITY IN BLIND

Electrophysiological procedures have demonstrated cross-modal plasticity in blind

humans, such that auditory 41, 42, 43 and tactile 43, 44, 45 stimuli are processed in visual areas of the

brain. This is evident by the cortical activation patterns and increased blood flow to these areas

(occipital cortex, cerebellum) during auditory and somatosensory discrimination tasks.

It is also been observed by electrophysiological mapping of the body representation in the

cortex of naturally blind mole rat that the occipital area normally occupied by the visual cortex

serves somatosensory function46.

Brain imaging studies describe the occurrence of visual cortex activity in blind people

during nonvisual tasks such as Braille reading, hearing words, or sensory discriminations of

tactile or auditory stimuli 47, 48.

The blind individuals showed activation of primary and secondary visual cortical areas

during tactile tasks, whereas the normal controls showed deactivation of these visual cortical

14
areas during similar tasks. Thus in blind subjects, cortical areas normally reserved for vision may

be activated by other sensory modalities like the somatosensory modalities49.

Experimental findings support the notion of altered capabilities for the surviving

modalities through reorganization of cortical functions. The possible mechanism for the

modifying activity in various parts of visual cortex of blind people is that the changes constitute

cross-modal plasticity in response to severe unimodal sensory deprivation. The potential

processes responsible for novel effects involve anatomical and physiological changes that have

been studied extensively using animal models 50.

Alternatively, observed access of surviving modalities to deprived cortex is an

expression, although exaggerated, of normal physiology that usually is inhibited or hidden when

vision is present. This potential mechanism relies on possible changes in the balance of activity

within existing cortical and sub cortical networks. These mechanisms are not mutually exclusive

at different ages for blindness onset and, therefore, for the differences in developmental sensitive

periods in establishing connections. Data from brain imaging studies especially will be potent in

revealing the network of active cortex to solve the confusion.

The occipital cortex in early onset blind (EB) individuals responds to a broad class of

stimuli from auditory and tactile domains and to a variety of cognitive tasks. For example,

functional magnetic resonance imaging (fMRI) and positron emission tomography studies have

established that medial occipital areas respond to a variety of stimuli and tasks42, 49, 51.

Study by Alho et al demonstrated participation of more posterior areas in generation of

potentials during auditory selective attention52.

Early "visual" cortex activation correlates with superior verbal memory performance in

the blind53.

15
 Changes in occipital cortex activity in early blind humans have also been studied using a

sensory substitution device54.

Röder et al. reported that an early negative evoked potential, the N1-evoked response, to

standard stimuli in an auditory oddball design had shorter latencies and larger amplitudes in EB

subjects than those of matched SC subjects. These shorter latencies may have reflected the

process by which EB achieve more rapid stimulus processing55.

Furthermore, the posterior shift in the distribution of the evoked potentials indicated that

recruitment of posterior temporal, parietal, and occipital cortices may have contributed to the

enhancement. Elbert et al argued that expansion of the tonotopic maps in primary auditory

cortex in blind individuals may account for some of the auditory perceptual advantages3.

Psychoacoustic studies have demonstrated that EB subjects outperform SC subjects on

56, 57 58
auditory spatial , spectral and temporal discrimination tasks59, as well as on more

complex attention and memory tasks 61, 62.

Modern brain imaging studies show that the visual cortex of congenitally blind and early-

blind individuals responds to a variety of tactile, auditory, and verbal tasks including Braille

reading 49. This cross-modal plasticity is thought to contribute to enhanced non-visual abilities in

people who are blind.

Recent data from brain imaging studies have shown that cross-modal interactions occur at

brain sites that used to be considered modality-specific. Calvert et al carried out a functional

magnetic resonance imaging (fMRI) study that showed that the primary auditory cortex is

activated when a talking face is viewed in the absence of sound. The activation was observed

specifically during speech or pseudo-speech type of lip movements63.

16
 Recent data showing rapid cross-modal plasticity in blindfolded, sighted subjects argue

against the establishment of new connections to explain cross-modal interactions in the blind.

Rather, the latent pathways that participate in multisensory percepts in sighted subjects might be

unmasked and may be potentiated in the event of complete loss of visual input64.

During non-Braille discrimination tasks, in blind subjects, the ventral occipital regions,

including the primary visual cortex and fusiform gyri bilaterally were activated while the

secondary somatosensory area was deactivated. The reverse pattern was found in sighted

subjects where the secondary somatosensory area was activated while the ventral occipital

regions were suppressed. These findings suggest that the tactile processing pathways usually

linked in the secondary somatosensory area are rerouted in

blind subjects to the ventral occipital cortical regions originally reserved for visual shape

discrimination65.

Study results suggest that activation of the visual cortex in blind subjects is related to

higher and more complex brain functions66.

Current descriptions of affected visual cortical regions differ, especially regarding

whether changes occur early in the hierarchy of visual brain areas, particularly in primary visual

cortex (V1), or arise in higher tier areas, some of which normally receive input from other

modalities. Some studies report V1 responses in early blind subjects (individuals who were born

blind or totally lost sight before age 6 49,65.Other studies indicate V1 activity mostly in late blind

subjects (individuals with sight at birth, who learned to read print, and who lost sight after age

12). The study observed activity throughout portions of visual cortex in all blind individuals

engaged in a Braille reading task, regardless of the age of blindness onset47.

17
 Contradictory findings suggest early blind individuals who usually read Braille better

than late blind individuals, have a greater visual cortical activity. The reorganizations noted in

the two populations; the early and late blind individuals are not identical, which indicates that

maturation and behavioral experience can influence and retain the adaptive potential of brain

areas47.

Some studies have shown that reorganization of primary motor and sensory cortex occurs

when there is unilateral extensive brain damage in the early gestational age67.

The visual cortex displays remarkable plasticity during development and is profoundly

influenced by visual experience. Depriving vision during a critical period of development when

visual experience has a maximum effect on the cortical structure will induce robust changes in

the anatomy and physiology of visual cortex 68.

AEP STUDIES IN THE BLIND

Throughout life specific, molecular, biochemical, electrophysiological and structural

changes take place in the central nervous system neurons and neuronal networks in response to

activity and behavior. Electrophysiological recordings obtained have revealed sharper tuning of

early spatial attention mechanisms in the blind subjects when compared with normal sighted

subjects1.

It is also been observed by electrophysiological mapping of the body representation in the

cortex of naturally blind mole rat that the occipital area normally occupied by the visual cortex

serves somatosensory function46.

18
 Electrophysiological procedures have demonstrated cross-modal plasticity in blind

humans, such that auditory41, 55,65and tactile stimuli 11, 44, 55

come to be processed in visual areas

of the brain. This is evident by the cortical activation patterns and increased blood flow to these

areas (occipital cortex, cerebellum) during auditory and somatosensory discrimination tasks.

The peak latency of the Pa wave (maximum positive peak between Na and 35 ms.) Nb

wave (the maximum negativity between 38 and 48 ms) and P100 wave of the MLAEP,the

N100, P200, and P300 wave of the LLAEP was significantly lower in the congenitally blind

group compared to normal vision group. 10,58,69,70

Another study had described a larger processing negativity (PN) to attended tones at

occipital scalp sites in CB subjects compared to subjects with normal vision. These results

suggested that in blind subjects in addition to the participation of conventional neural areas

(auditory cortex, frontal cortex) the parietal and even occipital cortices may contribute to the

PN52.

A study of the long-latency auditory event related potentials (ERPs) in early blind

humans showed that the negative deflection 100 ms from stimulus onset (NI00) and subsequent

deflections (P200 and P300) show shortened latencies and enhanced amplitudes58.

The N400 effect had a left-lateralized fronto-central scalp distribution in the sighted but a

symmetric and broad topography in the blind. Furthermore, the N400 effect started earlier in the

blind than in the sighted. Closed class compared to open class sentence middle words elicited a

more pronounced late negativity in the blind than in the sighted. These results suggest that blind

people process auditory language stimuli faster than sighted people and that some language

functions may be reorganized in the blind71.

19
 Marked plasticity changes were reflected in late auditory attentional processing (attend-

ear targets), in the form of a prolonged negativity (200-450 ms post-stimulus) that was absent in

the sighted subjects. The plasticity changes in the blind had a time course indicating progressive

recruitment of parietal and then occipital regions, providing new evidence for cross-modal

sensory reorganization in the blind7.

Targets elicited larger and more posteriorly distributed N2 responses in the blind than in

the sighted. Since target detection times were shorter in the blind as well, these findings imply

compensatory adaptations within the auditory modality in humans blind from birth57.

The P300 complex, on the other hand, which is a slow positive deflection over the

posterior part of the scalp and which follows rare and task-relevant events 200–800 ms after

stimulus onset was significantly smaller at occipital electrodes in the blind than in the sighted

subjects. The data cast doubt on the hypothesis that the occipital cortex of blind subjects

participates in modality-specific72.

20
 METHODOLOGY

SAMPLE SIZE:

The sample used in this study consisted of 40 Subjects-20 totally blind females and 20

age matched normal sighted females.

SAMPLING PROCEDURE:

Our study was a comparative study in which 20 totally blind females were recruited from

school for the blind and from those attending outpatient departments at M. S. Ramaiah Medical

and Teaching Hospital, Bangalore. 20 age matched normal sighted females from the general

population were studied as controls.

ETHICAL CLEARANCE:

Ethical clearance was obtained from the M. S. Ramaiah Medical College ethical

committee for human research to conduct the study.

Inclusion Criteria:

1) Subjects with congenital blindness.

2) Subjects with total blindness (Category-5) of >2 years73.

3) Age of individuals between 18 to 40 years.

4) Subjects in the early phase (the first week) of menstrual cycle.

21
Exclusion Criteria:

a) Subjects with other visual defects and other causes of blindness.

b) Subjects with history of hearing impairment.

c) Subjects with any other neurological disorders.

d) Subjects using any drugs – narcotics, stimulants and neurotropic drugs.

METHOD OF COLLECTION OF DATA:

Subjects were 20 females with Total Blindness and 20 females with Normal vision in the

age group 18- 40 years, in the early phase of menstrual cycle (within the first week of onset of

menstruation) and who satisfy the inclusion and exclusion criteria. Subjects were recruited and

examined from school for the blind and from those attending OPD at M.S.Ramaiah Medical and

Teaching Hospital from January 2009 to January 2010.

Subjects were assigned to two different groups - (A) Normal sighted females.

(B) Totally blind females

Ophthalmologist certified them for blindness through ophthalmologic and fundoscopy

examinations.

Totally Blind and normal sighted females were also screened for hearing threshold by

audiometry. Personal details like menstrual history and last date of previous menstrual cycle was

procured through history from all subjects.

22
 Subjects were screened for general physical health to rule out any clinical disorder likely

to interfere with the study findings. Anthropometrical details like weight in kilograms, height

and head circumference in centimeters were recorded from all the subjects.

Informed written consent was obtained from all subjects.

PARAMETERS USED FOR COMPARISON:

a) The peak latency of Na, Pa and Nb components of MLAEP.

b) The peak latency and amplitude of P300 wave.

10-20 international system for placing electrodes

23
PROCEDURES AND EQUIPMENT:

This study involved noninvasive procedures undertaken by all the subjects, both the

totally blind and normal sighted females as listed below. There was no financial liability on the

subjects, both the Totally Blind and the Normal sighted females for any of the investigations and

procedures performed.

AEPs (Auditory Evoked Potential) were recorded with the subjects awake, comfortably

lying down in the bed in a semi-darkened room and were requested to remain calm keeping their

eyes closed to avoid electro-oculographic artifacts due to eye movements and improve the

concentration and attention to the stimuli presented.

AEP Recordings were performed in an air conditioned, sound-proof room by using

Ag/AgCl disc electrodes affixed with Ten 20 conductive paste after cleaning the sites with

Nuprep EEG & ECG abrasive skin prepping gel at left and right ear lobules (A1,A2), Fz, vertex

(Cz) ,Pz and Oz for the recording of P300 and at Cz alone for MLAEP recording. Grounding

was done by placing an electrode on forehead (FPz). All electrodes were plugged to a junction

box and skin to electrode impedance was kept below 5 KOhm.

The acoustic stimulus parameters used for MLAEP acquisition were 1500 alternating

condensation and rarefaction click stimuli were delivered at 80 dB sound pressure level

monaurally through shielded headphones. Contralateral ear was masked with a white noise of –

24
30 dB. Signals picked up by electrodes were filtered (10 Hz and 200 Hz), amplified, averaged

and displayed on the screen of GALILEO NT Evoked Potential Recorder.

P300 was measured from the vertex (Fz, Cz, Pz and Oz) in response to random stimuli

presented mono-aurally through headphones applied to the subject's ear. The ground electrode

was placed at FPz. Standard auditory odd ball paradigm was used. In this paradigm design, the

subject was presented with 300 stimuli as a sequence of two distinguishable sound stimuli, one

of which occurred frequently (frequent stimulus /non-target) for 240 times and the other

infrequently (rare stimulus/target) for 60 times. The frequency of the frequent stimulus was

1000Hz and that of the rare stimulus was 2000Hz.

The subjects were instructed to press the button whenever a target/ infrequent stimulus

were presented as soon as possible. The stimulus sequence was random. The stimulus was

presented at 80 dB SPL. The settings were properly selected and evoked responses to the rare

stimuli were filtered with a band pass 1-30 Hz and averaged. Samples contaminated with

artifacts were auto discarded. The latency of N100, P200, N200, P300 and amplitude of waves

P200 and P300 for target stimuli (rare) were calculated. The responses to the frequent and rare

stimuli were averaged. The wave form pattern was replicated. The different wave form latencies

and amplitudes were calculated. Amplitude (µV) was measured from the peak of one polarity to

the immediately following peak of the opposite polarity.

Electrode placing, nomenclature and methodology of AEP recordings were according to

Chiappa (1990)74.

25
STATISTICAL METHODS:

Descriptive statistical analysis has been carried out in the present study. Results on

continuous measurements are presented on Mean ± SD (Min-Max) and results on categorical

measurements are presented in Number (%). Significance is assessed at 5 % level of

significance. Student t test (two tailed, independent) has been used to find the significance of

study parameters on continuous scale between two groups (Inter group analysis). Effect size has

been computed.

1: Fisher Exact test

Let there exist two such variables and , with and observed states, respectively. Now form a

matrix in which the entries represent the number of observations in which and .

Calculate the row and column sums and , respectively, and the total sum

of the matrix. Then calculate the conditional probability of getting the actual matrix given the

particular row and column sums, given by

which is a multivariate generalization of the hypergeometric probability function.

26
2. Chi-Square Test

χ 2
=
∑ (Oi − Ei) 2

, Where Oi is observed frequency and Ei is Expected frequency

Ei

Follows chi-distribution (r-1) x (c-1) df

3. Student t test (Two tailed, independent)

( x 1 − x 2 ) − ( μ1 − μ 2 )
t=
s 2 (1 / n1 + 1 / n2)

n1 n2
(n1 − 1)∑ ( x1 − x1) 2 + (n 2 − 1)∑ ( x 2 − x 2) 2
i =1 i −1
Where s 2 =
n1 + n 2 − 2

4. Effect Size

mean1 − Mean 2
d =
PooledSD

No effect (N) d<0.20

Small effect (S) 0.20 <d<0.50

Moderate effect (M) 0.50 <d<0.80

27
 Large effect (L) 0.80<d<1.20

Very large effect (VL) d>1.20

5. Significant figures  

+ Suggestive significance (P value: 0.05<P<0.10)

* Moderately significant (P value: 0.01<P ≤ 0.05)

** Strongly significant (P value: P≤0.01)

Statistical software: The Statistical software namely SPSS 15.0, Stata 8.0, MedCalc 9.0.1 and

Systat 11.0 were used for the analysis of the data and Microsoft word and Excel have been used

to generate graphs, tables etc.

Limitations in the methodology used:

1. Brain imaging techniques like fMRI would be better and more reliable. But for the current

study, they were unavailable and also not cost effective.

2. Study in both the sexes and to include both the early and late blind individuals would be

preferable.

28
 RESULTS

This Comparative case –control study consisted of 20 normal sighted individuals (Group

A) and 20 totally (congenital) blind (Group B). The significance of the latency and amplitude of

MLAEP and P300 waves of the auditory evoked potentials of the two groups were compared.

Two tailed independent t test was used to find the significance of difference in the basic

characteristics (Age, height, weight, head circumference, number of days from the last menstrual

period-LMP) between the two groups -Group A, Group B.

Effect size of blindness on right and left sides was determined statistically.

The basic characteristics did not show significant difference between the two groups (p >

0.05). The two groups were similar in terms of the basic characteristics (Table-1, 2, 3 & graph 1,

2, 3, 4, 5, 6).

The mean latency of MLAEP waveforms Na, Pa and Nb in the blind subjects for the right

and left ears were 22.78±1.86 ms, 28.7±4.22 ms, 35.99±3.36 ms and 23.64±2.28 ms, 30.12±4.28

ms, 38.64±4.03 ms, and in the normal subjects were 26.02±1.73 ms, 33.06±3.31 ms, 38.81±3.69

ms and 26.48 ±2.08 ms, 32.79 ±3.54 ms, 40.53±3.47 ms respectively. (Table-4)

Thus the mean pattern of absolute latencies of MLAEP waveforms Na, Pa and Nb from

right and left ears showed significant difference between the two groups with the blind subjects

having a decreased latency period compared to the normal subjects

(p< 0.001). (Table-4, Graph-7)

The mean latency of P300 waveform at Fz, Cz, Pz and Oz in the blind subjects was

311.97±5.08 ms,313.37 ± 5.42 ms,311.46 ±5.27 ms,312.61±4.51 ms and in the normal subjects

29
was 334.7 ± 11.53 ms,336.26 ±13.09 ms,338.67 ±12.94 ms,340.82 ±11.9 ms respectively.

(Table-6)

The mean pattern of absolute latency of P300 wave ( Fz, Cz, Pz, Oz ) showed

significant difference between the two groups with the blind subjects having a decreased latency

period compared to the normal subjects (p< 0.001). (Table-6, Graph-10)

The effect size showed variable relationship among the two groups for MLAEP latencies

while for the P300 latencies showed a very large effect between the two groups. (Table 4, 6)

The mean pattern of amplitude of MLAEPs (Na, Pa, Nb) in the blind subjects for the

right and left ears was 0.68±0.36 µv, 0.51±0.38 µv, 0.47±0.33 µv and 0.71±0.42 µv, 0.44±0.40

µv, 0.58±0.46µv and in the normal subjects was 0.79±0.62 µv, 0.61±0.43 µv, 0.71±0.45 µv and

0.80±0.52 µv, 0.49±0.43 µv, 0.73±0.50 µv respectively. (Table-5, Graph-8).

Thus the mean pattern of amplitude of MLAEPs (Na, Pa, Nb) did not show any significant

difference between the two groups (p > 0.05) except for Nb wave where it showed some

significance. (P value: 0.05<P<0.10)

The mean pattern of amplitude of P300 wave ( Fz, Cz, Pz, Oz) showed significant

difference between the two groups only at Oz (p < 0.05) where the amplitude of P300 waveform

was significantly increased in the blind subjects than in the normal subjects. (Table-6, Graph-

9).

The effect size showed mild to moderate relationship among the two groups for MLAEP

amplitudes while for the P300 amplitudes showed moderate effect between the two groups at Oz

site. (Table 5, 6)

30
 Table 1: Age distribution of subjects studied

Group A Group B
Age in years
No % No %

19-20 8 40.0 9 45.0

21-30 7 35.0 6 30.0

31-40 5 25.0 5 25.0

Total 20 100.0 20 100.0

Fig 1: Comparison of age distribution of subjects between the two groups

31
Table 2: Age, Height and Weight and Head circumference of subjects studied

Basic variables Group A Group B P value

Age in years 24.33±6.29 26.05±6.59 0.409

Height in cm 157.80±4.58 156.65±5.79 0.490

Weight kg 54.55±8.14 56.60±7.94 0.425

Head circumference cm 30.75±1.11 30.60±1.19 0.683

35

30

25
Age in years

20

15

10

0
Group A Group B

Fig 2: Comparison of age between the two groups

32
 164
162
160
158

Height in cm
156
154
152
150
148
146
144
Group A Group B

Fig 3: Comparison of height between the two groups

70

60

50
Weight kg

40

30

20

10

0
Group A Group B

Fig 4: Comparison of weight between the two groups

33
 32.5

32
Head circumference cm
31.5

31

30.5

30

29.5

29

28.5

28
Group A Group B

Fig 5: Comparison of Head circumference between the two groups

34
 Table 3: Number of days from LMP

No of days Group A Group B

from LMP No % No %

1 0 - 2 10.0

2 0 - 3 15.0

3 7 35.0 5 25.0

4 6 30.0 2 10.0

5 5 25.0 4 20.0

6 1 5.0 3 15.0

7 1 5.0 1 5.0

Total 20 100.0 20 100.0

50
45
40
35
Percentages

30
25
20
15
10 Group A
5 Group B
0
1 2 3 4 5 6 7
No of days from LMP

Fig 6: Number of days from LMP

35
 Table 4: Comparison of MLAEP LATENCY between the two groups

MLAEP-Latency in
Group A Group B P value Effect size
ms

RIGHT SIDE

Na 26.02±1.73 22.78±1.86 t=5.715;p<0.001** 1.77

Pa 33.06±3.31 28.7±4.22 t=3.643;p=0.001** 1.13

Nb 38.81±3.69 35.99±3.36 t=2.522;p=0.016* 0.78

LEFT SIDE

Na 26.48±2.08 23.64±2.28 t=4.105;p<0.001** 1.27

Pa 32.79±3.54 30.12±4.28 t=2.153;p=0.038* 0.67

Nb 40.53±3.47 38.64±4.03 t=1.594;p=0.119 0.49

* Significance at 5% ** Significance at 1%

50
45
MLEP-Latency in ms

40
35
30
25
20
15
10 Group A
5 Group B
0
Na Pa Nb Na Pa Nb

RIGHT SIDE Left side

Fig 7: Comparison of MLAEP LATENCY between the two groups

36
MLAEP-Amplitude
Group A Group B P value Effect size
(microvolt)

RIGHT SIDE

Na 0.79±0.62 0.68±0.36 t=0.663;p=0.511 0.21

Pa 0.61±0.43 0.51±0.38 t=0.771;p=0.446 0.24

Nb 0.71±0.45 0.47±0.33 t=1.886;p=0.067+ 0.58

LEFT SIDE

Na 0.80±0.52 0.71±0.42 t=0.565;p=0.575 0.18

Pa 0.49±0.43 0.44±0.40 t=0.397;p=0.693 0.12

Nb 0.73±0.50 0.58±0.46 t=0.965;p=0.341 0.30

Table 5: Comparison of MLAEP AMPLITUDE between the two groups

1.6

1.4
MLEP-Amplitude (mv)

1.2

0.8

0.6

0.4
Group A
0.2
Group B

0
Na Pa Nb Na Pa Nb

RIGHT SIDE Left side

Fig 8: Comparison of MLAEP AMPLITUDE between the two groups

37
 Table 6: Comparison of P300 (amplitude and Latency) between two groups

P300 Group A Group B P value Effect size

AMPLITUDE

(microvolts)

Fz 6.83±2.09 6.24±3.96 t=0.584;p=0.562 0.18

Cz 7.82±2.30 7.83±3.51 t=0.008;p=0.994 0.00

Pz 8.65±2.68 9.60±5.27 t=0.715;p=0.479 0.22

Oz 8.76±2.55 12.51±6.08 t=2.544;p=0.015* 0.79

LATENCY(ms)

Fz 334.7±11.53 311.97±5.08 t=8.069;p<0.001** 2.50

Cz 336.26±13.09 313.37±5.42 t=7.227;p<0.001** 2.24

Pz 338.67±12.94 311.46±5.27 t=8.712;p<0.001** 2.70

Oz 340.82±11.9 312.61±4.51 t=9.912;p<0.0001** 3.07

* Significance at 5% ** Significance at 1%

38
 20
18
16
14
12

P300
10
8
6
4 Group A
2 Group B
0
Fz Cz Pz Oz

AMPLITUDE

Fig 9: Comparison of P300 amplitude between two groups

360

350

340

330
P300

320

310

300
Group A
290
Group B
280
Fz Cz Pz Oz

LATENCY

Fig 10: Comparison of P300 amplitude between two groups

39
 DISCUSSION

Blind individuals have to rely on non visual information to a greater extent than the

sighted to efficiently interact with the external environment and consequently exhibit superior

skills in their spared modalities.

In our study we found results which were in agreement with our hypothesis that there is

neurophysiologic evidence of much better information processing in the auditory system due to

increased nerve conduction velocities in the blind and that the visual cortex also participates in

hearing in the totally blind compared to the normally sighted individuals suggestive of cross-

modal plasticity.

The mean pattern of absolute latencies of MLAEPs (Na, Pa, and Nb) showed significant

decrease in the blind when compared to the normal subjects (p < 0.001). This implies that there

is facilitation of processing of auditory information at the level of the diencephalic and the

superior temporal cortex (Heschl's gyrus) which are known to be the generators of the middle

latency waveforms75. This finding was similar to that done by Manjunath K et al and Naveen, et

al where they found that the peak latencies of both the Pa (maximum positive peak between Na

and 35 ms.) and Nb (maximum negative peak between 38 and 52 ms) waves was significantly

shorter in the congenitally blind compared to the normal sighted subjects10,70 .

We measured the base to peak (baseline to peak) and peak to peak (peak of one polarity

to the immediately following peak of opposite polarity) of all AEPs-Pa, Na, Nb and P300 for the

amplitude of the waves. Both of these two methods are commonly used. There is no good reason

to choose one or the other except the difficulty in defining the baseline sometimes makes that

measurement more subjective than the peak to peak method.

40
 The mean pattern of amplitude of MLAEPs (Na, Pa and Nb) did not show any

significant difference between the two groups (p < 0.001) for except for Nb wave where it

showed some significance (P value: 0.05<P<0.10) which is in contrast to the study by Naveen et

al which showed that the peak amplitude of the Pa wave recorded from the occipital area of the

congenitally blind subjects was significantly less than that of the normal sighted subjects,

recorded from the same site10. It appears that in the blind subjects’ changes in the generators of

the middle latency auditory evoked potentials are mainly related to latency rather than to the

scalp distribution of these components.

The mean pattern of absolute latency of P300 wave (Fz, Cz, Pz, and Oz) showed

significant decrease in the blind subjects when compared to the normal subjects (p < 0.001).This

probably indicates that the rate of automatic processing and information categorization is faster

in the blind subjects because of sensory compensation. It seems that neural plasticity increases

the rate of auditory processing and attention in early blind subjects. The latency of the late

cortical potentials(P300) provides information on the whole sensorium and its timing. This

finding is in agreement with V Niemeyer et al, Röder et al, Neville and Bavelier, Stevens and

Weaver and Fatemeh Heidari et al1, 10, 50,58,60,76.

The mean pattern of amplitude of P300 wave ( Fz, Cz, Pz and Oz) showed significant

difference between the two groups only at Oz where the amplitude was significantly more in the

blind subjects than in the normal subjects (p < 0.05). This posterior shift in the distribution

of the evoked potentials indicates that there may be recruitment of posterior temporal, parietal

and occipital cortices in auditory processing suggestive of cross-modal plasticity. These findings

41
go in agreement with that of Röder et al who found that the targets elicited larger and more

posteriorly distributed N2 responses in the blind than in the sighted1.

Such an observation in our study suggests the way in which the brain reorganizes itself in

response to blindness, possibly as a result of the blind individuals’ greater attention to and

reliance on nonvisual sensory avenues to maintain interaction with the world around him. These

findings are probably linked to increased attention and hence quicker processing during the

discrimination tasks of the event related potentials.

Focused attention on behaviorally relevant stimulation over extended periods has been

found to produce a substantial enlargement in the representational zones of the involved portions

of the body in somatosensory cortex in research with animals21, 26 and humans 34, 35
. Similarly,

the primary auditory cortical fields can be dramatically refined or profoundly degraded. Use-

dependent reorganization in the frequency receptive fields has been demonstrated by a number of

groups76, 78, 79.

Increasing interest has been devoted to the phenomenon of cross- modal plasticity in

blind humans, such that auditory 8, 9, 42, 52 stimuli come to be processed in visual cortex.

This plastic reorganization could result from an increase in the effectiveness of pre-

existing pathways, suggesting that the representational plasticity is a consequence of the heavy

differential sensory input.

There are two possible mechanisms for modifying activity in various parts of visual

cortex of blind people. One is that the changes constitute de novo cross-modal

plasticity in response to severe unimodal sensory deprivation. The potential

processes responsible for novel effects involve anatomical and physiological changes that

have been studied extensively using animal models50.Alternatively, observed access of

42
surviving modalities to deprived cortex is an expression, although exaggerated, of normal

physiology that usually is inhibited or hidden when vision is present. This

potential mechanism relies on possible changes in the balance of activity within existing

cortical and subcortical networks. These mechanisms are not mutually exclusive given

different ages for blindness onset and, therefore, differences in developmental sensitive

periods in establishing connections.

Thus our study provides evidence of neuroplasticity changes such as increased nerve

conduction velocity causing better information processing in the auditory system in the blind

.There is also neurophysiological evidence for the visual cortex participating in hearing in the

totally blind compared to the normally sighted individuals suggestive of cross-modal plasticity .

This finding can guide future studies of the cellular and molecular mechanisms important in

neuroplasticity. Additionally, in the long run, they may contribute to the design of educational

and rehabilitative programs for the blind.

43
 SCOPE FOR FUTURE STUDY

1) To study the effect of onset of blindness on the human nervous system which may allow us to

define sensitive periods for the multiple aspects of human vision and provide insight into the

complex interactions between neurodevelopment and environmental input.

2) To study in both sexes would be preferable.

44
 CONCLUSION

1. The totally blind individuals had significantly reduced latencies suggestive of increased

nerve conduction velocity leading to much better information processing in the auditory

system.

2. The totally blind individuals have larger P300 amplitude more posteriorly which is

suggestive of the visual cortex being activated for auditory stimulation. This indicates that

there is cross-modal plasticity.

45
 SUMMARY

We studied the changes in the auditory cortex in 20 totally blind and compared it with 20

age matched normal females by recording MLAEP and P300.

The mean latencies and amplitude of the waveforms Na, Pa, Nb of MLAEP and P300

were measured. The results were compared between the two groups. The mean latencies of all

the waveforms were significantly reduced in the blind subjects compared to the normal subjects.

The mean amplitudes of the waveforms Na, Pa, Nb did not show any significant changes

between the two groups. The mean amplitude of the waveform P300 at Oz site was significantly

increased in the totally blind.

This experiment suggests that the totally blind individuals demonstrate remarkable

neuroplastic changes such as increased nerve conduction velocity causing better information

processing in the auditory system in the blind .There is also neurophysiological evidence for the

visual cortex participating in hearing in the totally blind compared to the normally sighted

individuals suggestive of cross-modal plasticity . This is a use dependent response of the totally

blind individuals’ reliance on nonvisual modalities.

46
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MLAEP RECORDING IN THE BLIND SUBJECT

MLAEP RECORDING IN THE NORMAL SIGHTED

57
 P300 RECORDING IN THE BLIND SUBJECT

P300 RECORDING IN THE NORMAL SIGHTED SUBJECT

58
GALILEO NT INSTRUMENT

59
SILVER CUP ELECTRODES

60
SILVER CUP ELECTRODES ATTACHED TO THE BOARD

61
 INFORMED CONSENT FORM

A COMPARATIVE STUDY OF THE MIDDLE LATENCY AND P300 RESPONSES OF THE

AUDITORY EVOKED POTENTIALS IN THE TOTALLY BLIND AND NORMAL
SUBJECTS

I Mr/ Mrs……………………………………........ aged ………………..years have been

informed in detail (verbal and written information) from the doctor regarding the study for
research purpose in my own language. The objective of the study is to compare the peak
latencies of Pa, Na and Nb waves of MLAEP and the peak latency and the amplitude of P300
wave in the totally blind and normal subjects.

There will be no financial burden on me. I here by give consent for the proposed study.

Signature of the patient:

Date:

Place:

62
 NO OF DAYS
HEAD

MLAEP AMPLITUDE IN MICROVOLTS P300 AMPLITUDE IN MICROVOLTS P300 LATENCY IN MILISECONDS

AGE IN HEIGHT IN WEIGHT CIRCUMFERANCE FROM MLAEP LATENCY IN MILLISECONDS

SL NO BLIND SUBJECTS GROUP SEX YEARS cm kg cms LMP right left right left

Na Pa Nb Na Pa Nb Na Pa Nb Na Pa Nb Fz Cz Pz Oz Fz Cz Pz Oz

1 YESUMAMMA MARINA B Female 20 148 45 29 3 0.72 0.27 0.79 0.08 0.3 0.5 25.27 31.75 37.12 20.41 27.44 36.02 3.58 5.18 8.67 6.14 305.86 307.81 305.86 305.86

2 SUMAIYYA KHAN B Female 20 156 53 30 5 0.35 0.04 0.4 0.52 0.14 0.2 23.69 26.59 35.65 22.22 32.11 42.25 3.23 9.85 4.09 17.6 313.67 305.86 305.86 305.86

3 MARY AGNES B Female 19 152 55 30 6 0.79 0.44 0.96 0.22 0.16 0.43 18.44 21.49 30.28 22.59 25.76 31.1 3.34 6.68 9.82 14 311.72 309.77 311.77 311.72

4 MONISHA B Female 20 162 45 28 3 0.29 0.57 1.27 0.57 0.56 1 20.19 22.9 39.05 20.39 22.95 38.95 3.66 7.93 9.33 9.17 311.72 315.63 309.77 307.81

5 ANNAMMA VARGHESE B Female 35 162 58 32 3 0.54 0.6 0.46 0.54 0.44 0.52 22.39 25.61 38.12 23.16 27.22 36.89 5.69 12.3 4.31 8.27 317.58 309.77 315.63 313.67

6 FARHANA BANU B Female 23 146 57 30 7 1.6 0.86 0.09 1.01 0.93 0.82 23.32 26.5 32.48 24.91 28.33 33.82 13.2 14.7 16 12.1 305.86 309.77 305.86 307.81

7 TAMIL SELVI B Female 20 155 56 30 5 0.71 0.13 0.67 0.8 0.09 0.29 22.12 27.61 33.42 21.37 26.62 34.43 6.33 3.14 9.9 4.22 311.72 313.67 313.67 311.72

8 VIJAYA LAKSHMI B Female 28 160 58 31 5 0.92 1.07 0.61 0.92 0.96 0.4 21.25 23.44 35.41 22.14 25.62 38.1 4.46 8.77 15.4 17.8 301.95 313.67 313.67 315.63

9 ANITHA B Female 20 148 50 30 6 1.24 1.63 0.37 1.32 0.8 0.62 24.54 30.4 37 24.65 29.78 39.06 7.12 6.06 8.13 10.1 307 313.67 309.77 311.72

10 ANTO MELVINA B Female 20 160 44 30 3 0.57 0.66 0.54 1.07 0.26 0.54 24.91 28.74 38.11 25.76 33.7 40.54 13.8 7.98 12 11.7 315.63 311.72 311.12 313.67

11 VASANTHA PREMA B Female 20 160 54 30 3 0.99 0.3 0.25 0.3 0.01 0.69 23.57 25.27 31.26 22.1 24.91 33.46 11.1 9.55 6.56 7.26 321.48 321.4 321.48 321.48

12 SATHYA B Female 19 148 55 31 3 0.67 0.42 0.14 0.61 0.22 0.71 21.61 29.05 34.28 24.3 29.67 40.2 10.1 7.47 10.6 21.6 317.58 317.58 315.63 317.58

13 SHALOM B Female 35 157 60 30 3 0.54 0.05 0.03 0.79 0.1 0.24 21.12 30.53 32.46 20.63 30.28 40.49 11.2 9.9 26.5 17.5 307.81 305.86 305.86 305.86

14 MEENAKSHI B Female 38 155 62 31 5 0.49 0.49 0.13 0.49 0.47 0.39 24.54 37.73 45.3 26.01 35.48 46.89 1.48 8.7 10.1 17.9 317.58 309.77 311.72 317.78

15 KALAMMA B Female 29 161 63 32 4 0.81 0.46 0.12 0.86 0.34 0.01 21.49 35.29 37.12 23.44 33.09 41.88 6.78 7.11 6.27 10.1 317.58 321.48 305.86 317.58

16 MUNIRATHNA B Female 29 165 63 33 5 0.39 0.34 0.81 0.52 0.25 0.18 21.49 35.29 37.12 26.18 36.87 43.22 2.47 1.89 3.33 5.46 311.72 311.72 309.77 317.58

17 SHEELAVATHI B Female 31 166 58 32 6 0.9 0.89 0.19 1.86 1.24 1.38 25.89 30.4 38.22 28.45 38.46 41.51 0.23 2.97 6.14 9.28 313.67 311.72 309 313.67

18 NETHRAVATHI B Female 30 158 53 31 3 0.18 0.32 0.27 0.2 0.1 0.16 22.59 30.28 37.36 22.28 29.17 39.1 3.13 10.3 11.4 9.82 307.81 327.34 325.39 311.72

19 SAVITHA B Female 30 158 45 30 5 0.05 0.25 0.75 0.49 0.04 0.56 23.67 26.74 36.87 25.52 35.41 41.88 4.69 2.83 8.45 11.4 307.81 315.63 307.81 309.77

20 RENUKA B Female 35 156 54 32 4 0.82 0.5 0.54 1.04 1.33 1.97 23.44 28.33 33.21 26.37 29.43 32.97 9.2 13.3 4.93 28.7 313.67 313.6 313.6 313.72
 HEAD
CIRCUMFE
SL. NO NORMAL GROUP SEX AGE HEIGHT WEIGHT RENCE cm NO OF MLAEP AMPLITUDE IN MICROVOLTS MLAEP LATENCY IN MILLISECONDS P 300 P300

YEARS cm kg cm DAYS RIGHT LEFT RIGHT LEFT AMPLITUDE IN MILLIVOLTS LATENCY IN MILLISECONDS

FROM LMP Na Pa Nb Na Pa Nb Na Pa Nb Na Pa Nb Fz Cz Pz Oz Fz Cz Pz Oz

1 ANAHITA KINI A Female 26 165 54 32 5 1.11 0.31 0.31 0.49 0.28 0.11 26.82 34.43 40.54 26.74 29.43 39.07 5.38 6.48 6.03 9.51 325.39 323.44 331.25 331.25

2 KAVYA KAUSHIK A Female 20 159 45 30 4 0.24 0.26 0.32 0.42 0.28 0.43 26.74 36.39 43.22 27.47 33.46 39.8 4.38 6.99 8.24 8.6 339.06 350.78 354.69 339.06

3 MEGHA A Female 19 156 65 33 6 0.36 0.11 0.04 0.48 0.2 0.12 22.83 29.06 38.83 26.86 35.53 40.9 8.53 9.65 6.4 5.58 339.06 335.16 339.06 341.02

4 SUGUNA A Female 19 149 40 29 7 1.06 0.16 1.08 0.94 0.34 0.74 26.13 29.43 32.23 24.3 30.04 32.11 4.56 7.24 9.1 9.66 333.2 331.25 321.48 337.11

5 SWATHI A Female 20 160 60 31 4 0.5 0.64 0.58 1.08 0.62 0.28 26.28 38.22 42.49 26.32 37.61 40.42 5.83 6.43 12.5 12.9 356.64 352.73 364.45 356.64

6 VIDHYASHREE A Female 20 158 47 30 3 0.14 0.25 0.32 0.28 0.24 1.87 24.3 28.57 34.8 24.42 27.84 36.26 8.87 9.55 13.7 8.79 321.48 321.48 321.48 321.48

7 THANYA A Female 22 157 46 30 5 0.79 0.77 0.63 1.32 0.09 0.95 26.86 35.78 44.08 24.66 32.84 45.3 7.29 12 11.6 7.44 333.2 337.11 337.11 333.2

8 DIANA RODRIGUES A Female 22 160 55 31 3 1.06 0.89 1.31 0.59 0.35 0.84 28.21 31.75 36.51 29.06 38.1 41.64 6.63 6.72 9.48 9.18 315.63 315.58 331.25 335.16

9 MANJURANJANI A Female 20 158 62 32 4 0.05 0.71 0.55 1.1 0.8 0.74 21.61 30.16 36.14 22.1 28.21 38.22 10.5 7.41 9.24 11.01 333.2 323.21 323.41 323.44

10 SANDYA A Female 21 148 50 30 5 0.48 0.31 0.4 0.41 0.54 1.83 25.52 32.72 34.55 25.14 32.23 35.16 9.83 9.3 6.92 4.02 331.25 337.11 333.2 339.06

11 SHWETHA REDDY A Female 20 150 44 30 3 2.68 1.61 1.25 1.85 1.91 0.54 25.64 29.06 32.32 26.5 30.4 43.71 5.75 8.26 9.78 13.9 360.55 362.5 354.69 358.59

12 SHARADHA REDDY A Female 23 160 66 32 3 1.7 1.49 0.59 2.27 7-Jan 0.75 27.23 36.02 40.42 27.47 33.09 39.8 3.61 2.97 6.37 6.99 337.11 337.11 337.21 335.16

13 SALMA MEHRUKH A Female 22 162 48 29 3 1.21 0.6 0.94 0.63 0.31 0.73 26.86 36.39 42.12 25.27 31.38 43.96 9.42 6.52 7.92 12.4 354.69 354.59 344.92 364.45

14 PAYAL KHANNA A Female 20 158 50 30 4 0.95 0.53 1.03 0.86 0.17 0.34 25.76 31.87 41.88 27.59 33.94 42.61 5.8 9.3 8.61 6.6 328.34 330.1 323.44 338.61

15 ANNU PRIYA A Female 21 164 52 30 3 1.2 0.25 1.91 0.54 0.08 1.43 28.33 34.43 39.8 28.57 34.07 41.27 8.61 6.67 4.28 6.05 327.34 315.63 323.44 337.11

16 SONY A Female 31 158 59 30 4 0.32 1.2 0.36 0.29 0.5 0.11 26.72 34.4 40 26.74 28.41 42.08 4.38 6.31 7.41 8.6 336.06 350.76 356 339.6

17 RATHNA A Female 38 154 66 31 5 0.24 O.26 0.38 0.48 0.28 0.52 28.22 35.78 39.66 30.42 40.81 44.02 8.8 9.55 13.7 8.8 322.23 337.21 352.4 338

18 MALA A Female 35 160 64 32 4 0.68 0.5 0.58 0.63 0.8 0.74 24 29.42 38.38 25.1 32.01 39.32 4.28 8.4 5.62 6.24 333.21 333 340.23 339

19 JOYCE A Female 32 162 56 32 3 0.38 0.48 0.51 0.54 0.41 0.6 26.28 38.11 43.4 30.04 36.21 46.24 6.64 4.29 6.06 8.08 337.11 342.97 344.92 342.78

20 SHANTHI A Female 36 158 62 31 5 0.56 0.93 1.02 0.7 1.2 0.86 26.04 29.3 34.82 24.78 30.14 38.78 7.41 12.42 10.08 10.78 329.33 333.46 338.81 365.76