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EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC NERVE IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE BY USING EVOKED POTENTIAL STUDY Dissertation submitted to THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY In partial fulfillment of the Regulation for the award of the degree of M.D. (PHYSIOLOGY) BRANCH – V THANJAVUR MEDICAL COLLEGE ,THANJAVUR THE TAMIL NADU DR.M.G.R.MEDICAL UNIVERSITY CHENNAI, INDIA MAY - 2018

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EVALUATION OF VESTIBULOCOCHLEAR NERVE

AND OPTIC NERVE IN CHRONIC OBSTRUCTIVE

PULMONARY DISEASE BY USING EVOKED

POTENTIAL STUDY

Dissertation submitted to

THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY

In partial fulfillment of the

Regulation for the award of the degree of

M.D. (PHYSIOLOGY)

BRANCH – V

THANJAVUR MEDICAL COLLEGE ,THANJAVUR

THE TAMIL NADU DR.M.G.R.MEDICAL UNIVERSITY

CHENNAI, INDIA

MAY - 2018

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CERTIFICATE

This is to certify that this Dissertation entitled “Evaluation of

Vestibulocochlear Nerve and Optic Nerve in Chronic Obstructive Pulmonary

Disease by Using Evoked Potential Study” is a bonafied work done by

DR.K.Anitcheady, under my guidance and supervision in the Department of

Physiology, Thanjavur Medical College, Thanjavur during her Post Graduate course

from 2015 to 2018.

Dr.S.JeyakumarM.s,Mch(Vascular),D.N.B,F.R.C.S(Edin) Dr.R.Vinodha, M.D.,

The Dean, Professor and HoD,

Thanjavur Medical College, Thanjavur Medical College,

Thanjavur – 613004. Thanjavur – 613004.

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ANTI – PLAGIARISM REPORT

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CERTIFICATE - II

This is to certify that this dissertation work titled Evaluation of

Vestibulocochlear Nerve and Optic Nerve in Chronic Obstructive

Pulmonary Disease by Using Evoked Potential Study of the candidate

Dr.K.Anitcheady with registration Number 201515201 for the award of M.D.,

in the branch of PHYSIOLOGY I personally verified the urkund.com website

for the purpose of plagiarism Check. I found that the uploaded thesis file

contains from introduction to conclusion pages and result shows 1 percentage

of plagiarism in the dissertation.

Dr.R.Vinodha, M.D.,

Professor and HOD,

Thanjavur Medical College,

Thanjavur – 613004.

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DECLARATION

I solemnly declare that this Dissertation “Evaluation of

Vestibulocochlear Nerve and Optic Nerve in Chronic Obstructive

Pulmonary Disease by Using Evoked Potential Study”was done by me in the

Department of Physiology, Thanjavur Medical College and Hospital, Thanjavur

under the guidance and supervision of my professor Dr.R.VINODHA, M.D.,

Department of Physiology, Thanjavur Medical College, Thanjavur between 2015

and 2018.

This Dissertation is submitted to the TamilNaduDr.MGR Medical

University. Chennai in partial fulfillment of University requirements for the

award of M.D.Degree(Branch - V) in Physiology.

Dr.K.Anitcheady

Postgraduate Student,

Thanjavur Medical College ,

Thanjavur – 4.

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ACKNOWLEDEMENT

I express my deep sense of gratitude to my beloved

Prof. Dr. R.Vinodha.MD, Professor of Physiology, my teacher and

my guide, who provided constant guidance and advice throughout

this study and without whose initiative and ethusiasm this study

would not have been completed.

I am extremely grateful to the Dean Thanjavur Medical

College for granting me permission to do this dissertation work in

Thanjauvr Medical College Hospital, Thanjavur.

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CONTENTS

S.NO Title Page No

1 INTRODUCTION 1

2 AIM OF THE STUDY 5

3 REVIEW OF LITERATURE 6

4 MATERIALS AND METHODS 59

5 RESULTS 65

6 DISCUSSION 82

7 CONCLUSION 89

8 BIBILOGRAPHY

9 ANNEXURES

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ABSTRACT

TOPIC:EVALUATION OF VESTIBULOCOCHLEAR NERVE AND

OPTIC NERVE INVOLVEMENT IN CHRONIC OBSTRUCTIVE

PULMONARY DISEASE BY USING EVOKED POTENTIAL STUDY.

The aim of the study is to evaluate the visual evoked potential (VEP) and

brainstem auditory evoked potential (BAEP) abnormalities in COPD patient and

its correlation with C-reactive protien (CRP) as a part of multi system disorder.

40 study group with chronic obstructive pulmonary diseases and 40

control group between the age group of 30-60 years were included in this study

based on criteria defined in the global initiative for chronic obstructive lung

disease (gold) 2004- guidelines.

Patients with chronic neuropathy without COPD diabetes mellitus,

chronic alcoholism, uremia, cystic fibrosis, sarcoidosis, leprosy, malignancy,

history of intake of neurotoxic drugs, hearing and visual impairment were

excluded.

Informed written consent from the study and control group were

obtained.

Result: There was significant prolongation of (P100) over the right eye in

COPD patients compared with controls. BAEP recording shows significant

prolongation of latency of wave I, II, III, IV and V over the left ear.

The indices of spirometry FVC, FEV FEV1/FVC, were significantly

decreased in COPD patients and CRP were significantly increased in COPD

patients when compared with control

Key words: VEP, BAEP, C-Reactive Protein, Chronic obstructive pulmonary

disease, Hypoxemia

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1

INTRODUCTION

The term chronic obstructive pulmonary disease (COPD) was

introduced to bring together a variety of clinical syndromes associated

with destruction of and airflow obstruction. The terms chronic obstructive

airways disease(COAD) and chronic obstructive lung disease (COLD)

have been used as synonyms in different parts of the world and chronic

obstructive pulmonary diseases (COPD) has been defined by the Global

Initiative for chronic obstructive lung disease (GOLD) as “a disease stage

characterized by air flow limitation that is not fully reversible”

Chronic obstructive pulmonary diseases includes (i) emphysema

defined as the permanent abnormal distension of the air spaces distal to

the terminal bronchioles accompanies by destruction of their wall without

fibrosis.

(ii) chronic bronchitis defined on the presence of chronic

productive cough on most days for 3 months in each of two consecutive

years.

(iii) small air way disease in which small bronchioles are

narrowed.

Excluded from this definition is Bronchial Asthma , chronic

Bronchitis and emphysema were frequently coexist since they share

common etiological factors and after many years chronic bronchitis get

complicated by emphysema.

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GOLD estimates suggested that chronic obstructive pulmonary

diseases, fourth most common cause of death world wide at present, will

be the third common cause of death world wide by 2020.

This disease is frequently seen in middle – aged subjects. Chronic

obstructive Pulmonary diseases affects male more frequently than

females because of smoking(1). It is equally prevalent in rural and urban

areas.

Increased smoking habits among younger people, increasing

urbanization, increasing automobiles and emergence of industries leading

to air pollution that has definite impact on the epidemiology of chronic

obstructive pulmonary diseases.(2)

Low birth weight, malnutrition recurrent respiratory infection in

childhood also predisposed of chronic obstructive pulmonary disease in

future.(3)

Spirometry is the most robust test of airflow limitation in patients

with chronic obstructive pulmonary diseases(4)

COPD is presently regarded as a multi – system disorder with

significant extra pulmonary manifestations in addition to its pulmonary

components. COPD patients displayed mild cerebral deficits, which are

related partially to pressure of arterial oxygen (Pao2) and to the degree of

pulmonary impairment.

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COPD patients suffered deficits on neurophysiological functioning

suggesting of organic mental disturbances and the rate of

neuropsychological deficit increased from 27% in mild hypoxemia to

61% in severe hypoxemia. Progressive hypoxemia leads to an increase in

blood viscosity and pulmonary vascular resistance which result in cor -

Pulmonale and a decrease in cerebral perfusion.

When Pao2 falls below 60 mmHg tissue hypoxia occurs and this

cause systemic effects. Accordingly visual and auditory receptors are

sensitive and more affected by hypoxemia.(5)

An evoked potential is an electrical potential recorded from the

nervous system of a human or other animal following presentation of a

stimulus, as distinct from spontaneous potentials as detected by electro

encephalography, & electromyography, or other electro physical

recording method.

VEP is a series of signals representing the response of the visual

occipital cortex to visual stimulus including flash and pattern stimuli and

can be used as one of the objective non-invasive neurophysiological

parameters in the assessment of the functions of visual organs, visual

pathways and the optical CNS.(6)

P100 latency is the representative component of VEPs and the most

commonly used index for its high, steady amplitude and slight intra and

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inter – individual variability of P100 latency of the VEP was defined as the

time from the stimulus onset to the main positive peak

Brainstem auditory evoked potentials (BAEP) are the potentials

recorded from the ear and vertex in response to a brief auditory

stimulation to assess the conduction through auditory pathway up to

midbrain(7)

The value of evoked potentials in assessing acute hypoxic state is

well established. However, its value in assessing the effect of chronic

hypoxic – hypercapnic states on mental function is not similarly well

defined and the results of different studies were inconsistent.

C - reactive protein (CRP) is an acute – phase protein synthesized

predominantly by hepatocytes in response to tissue damage or

inflammation. It reflects the total systemic burden of inflammation of

individuals and has been shown to be increased in COPD in stable

condition and during exacerbation.(8)

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AIM AND OBJECTIVE OF THE STUDY

1. To assess the functional integrity of visual pathway by using visual

evoked potential (VEP) in COPD.

2. To assess the functional integrity of auditory pathway by using Brain

stem Auditory evoked potential (BAEP) in COPD

3. Pulmonary function Test (PFT) in COPD.

4. To correlate parameters of PFT with BAEP &VEP.

5. To correlate the level of C-Reactive protein(CRP) with PFT, VEP and

BAEP parameters.

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REVIEW OF LITERATURE

Prior to 1979, patients with these conditions were often classified by

symptoms (chronic bronchitis, chronic asthma) by pathological

changes(emphysema) or by physiological correlates (pink puffers,blue

bloaters).Recognition that these entities overlapped and often coexisted

led to the term COPD.

Recently it has been realized that COPD is associated with a number

of co-morbidities, e.g. ischemic heart disease, hypertension, diabetes,

heart failure and cancer, suggesting that there is a generalized systemic

inflammatory process.

In 1956 the Medical Research Council in its journal used the term

chronic bronchitis to describe conditions with chronic cough with

expectoration of bronchial mucus hyper secretion. When other causes like

TB, PT Bronchiectasis were excluded.

In 1959 Higgins established the clear relationship between “smoking

and persistent cough and sputum production.

In 1960 gross and associates leads to the proteinase and antiproteinase

hypothesis in emphysema observed in ∝� antitrypsin deficiency.

COPD is a multisystem disorder that is frequently associated with

significant extra pulmonary manifestations. Peripheral neuropathy is

known to occurs as a systemic manifestation of COPD and the optic

nerve may also be affected due to the same manifestation Gupta et al.

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Atisetal reported BAEP and VEP abnormalities. In late 1960 owen

and campell et al observed the pathological changes in airways due to

cigarette smoking.

In 1973 Bougly and colleagues published a series of papers on

prognosis factors in chronic obstructive pulmonary diseases and

prognosis values of lung function test in chronic obstructive pulmonary

diseases.

Fig.1 Front Chest Xray in Normal Patient & COPD

EPIDEMIOLOGY& AETIOLOGY

COPD is caused by long-term exposure to toxic particals and

gases. In developed countries, cigarette smoking accounts for over 90%

of cases. In developing country factors such as the inhalation of smoke

from biomass fuels used in heating and cooking in poorly ventilated

areas, are also implicated.(10)

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However, only 10-20% of heavy smokers develop COPD,

indicating individual susceptibility. The development of COPD is

proportional to the number of cigarettes smoked per day; the risk of death

from COPD in patients smoking 30 cigarettes daily is 20 times that of

non-smoker. Autopsy studies have shown substantial numbers of

centriacinar emphysematous spaces in the lungs of 50% of smokers over

the age of 60 years independent of the diagnosis of significant respiratory

disease before death.

Climate and air pollution play a major role in urbanization, social

class and occupation may also play a part in aetiology, but these effects

are difficult to separate from that of smoking.The scocio-economic

burden of COPD is considerable.

PREVALENCE IN INDIA

Chronic obstructive pulmonary diseases is the second most

common lung disorder after pulmonary tuberculosis.(11)

Incidence are higher in males due to higher of smoking. It is a

disease of middle aged and elderly people, less common below the age of

35yrs.

Studies from North India, reported that the prevalence of chronic

bronchitis was as high as 16% in people above 40 yrs from rural areas.

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Prevalence is more in North India than South India due to seasonal

variability, particularly extremes of climate in North India.

MORTALITY DUE TO CHRONIC OBSTRUCTIVE

PULMONARY DISEASE

Chronic obstructive pulmonary disease (COPD) is a growing

global epidemic that is estimated to kill around three million people every

year. It is currently the fourth largest killer disease in the world and

expected to climb to the third position by the year 2030.

The number of deaths due to coronary heart disease, stroke and

other cardiovascular diseases have reduced substantially over the years,

whereas COPD is the only disease whose mortality rates have increased

substantially.

The WHO has estimated that mortality rate, due to COPD will

increase by around 60% in the southeast Asian region over the next two

decades. (12)

MORBIDITY DUE TO COPD:

COPD is a common and leading cause of worsening of quality of

life. The world health organization (WHO) has estimated that 600millions

people worldwide have COPD.

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RISK FACTORS:

SMOKING

Pipe and cigar smokers have a higher mortality and morbidity

rates, COPD shows a dose response relationship with the number of pack-

years of tobacco consumed.

British Thoracic society guidelines suggest that most patients with

COPD have at least 20 pack year smoking history

An average cigarette smoker have high annual rate of decline

FEV1 of about 50ml; in non-smokers the decline in FEV1 begins at 30-

35yrs of age and this may occur earlier in smokers.(13)

Stopping cigarette smoking does not produce a substantial

improvement in FEV1 but the subsequent rate of decline is decreased.

Prolonged cigarette smoking and impaired respiratory epithelial

ciliary movement, inhibits the function of alveolar macrophages & leads

to hyperplasia and hypertrophy of mucus secreting glands. Cigarette

smoke also inhibits anti proteases and cause polymorphonuclear

leukocytes to release proteolytic enzymes. Smoking is associated with

increased airway responsiveness, which is associated with more rapid

progression in patients with COPD. Obstruction of small airway is the

earliest demonstrable mechanical defect in a smoker.

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AIR POLLUTION

Incidence and mortality rates of both chronic bronchitis and

emphysema may be higher in industrialized urban areas. Exacerbation of

bronchitis are clearly related to periods of heavy pollution with sulfur

dioxide and particulate matter.

In developing countries like India traditional working fuels such as

wood, cow dung cake, etc along with poorly ventilated houses are

significant risk factors for chronic bronchitis

SOCIO ECONOMIC STATUS

Hrubec et al found a strong association between socio economic

status based on occupation and respiratory symptoms in a study of twins.

In so many studies it was observed that an inverse relation between

percapita income &obstructive lung disease.

OCCUPATION:

Chronic bronchitis is more prevalent in workers who engage in

occupation exposing them to either inorganic or organic dusts, or to

noxious gases. Surveys have found accelerated decline in lung function in

such workers (eg) workers in plastic plants to exposure to toluene

disorganate etc. Exposure to cadmium can increase the change of

development of emphysema and hence COPD.(14)

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RECURRENT RESPIRATORY INFECTIONS:

Frequency of acute respiratory illness are higher in patients with

chronic bronchitis. Epidemiological studies however implicate recurrent

respiratory illness as one of the major factors associated with etiology as

well as progression of chronic airway obstruction.(15)

AIRWAY HYPER RESPONSIVENESS AND ATOPY:

Even though airway hyper responsiveness is a feature of asthma

many patient with COPD also share this feature but less than 15% of

reversibility of obstruction to bronchodilators.

GROWTH AND NUTRITION:

Studies have shown that nutrition may affect both the growth and

decline in ventilator function. There is also some evidence that severe

viral pneumonia early in life may lead to chronic obstruction particularly

in small airways.

GENETIC FACTORS:

∝� ANTITRYPSIN DEFICIENCY:

∝� antitrypsin (∝� AT) is a polymorphic glycoprotein responsible

for the majority of anti-protease activity in the serum, whose synthesis is

governed by a gene on 14q 32 chromosome. The most commonest

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deficient allele termed ZZ (corpiZZphenotype I) results from a single

amino acid substitution 342 Glu-Lys. Which cause spontaneous

polymerization of the polypeptide, markedly impairing its release into,

circulation from the liver.

It is commonly seen among people from europeon descent 1:2000

to 1:7000 people, rate in people from African and Asian leniage. ∝� AT

deficiency accounts for 2% of observe cases of emphysema, patients

present with premature development of emphysema, chronic bronchitis.

The patient usually present with cough and dyspnea in the fourth decade.

Nearly 80% had a family history of lung disease with autosomal recessive

inheritance .

The average decline of FEV1 is 100-300ml/yr for smokers and 50

to 80ml/yr for ex-smoker of lifetime nonsmokers.

Pathologically panacinar emphysema predominates and

radiographically changes are most marked in lower lobes. Tobacco

smoking is an extremely important cofactor for development of disease in

∝� AT deficiency. These patients are also at increased risk of hepatic

cirrhosis.(16)

• Pathological changes characteristic of COPD are found in the

proximal airways, peripheral airways, lung parenchyma, and

pulmonary vasculature. These changes include chronic

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inflammation, and structural changes resulting from repeated injury

and repair.

• Inhaled cigarette smoke and other noxious particles cause lung

inflammation, a normal response which appears to be amplified in

patients who develop COPD.

• There is a characteristic pattern in inflammation in the lungs of

COPD patients, with increased numbers of neutrophils (in the

airway lumen), macrophages(airway lumen, airway wall, and

parenchyma), and CD8+ lymphocytes (airway wall and

parenchyma). The pattern is different from that seen in asthma.

• Lung inflammation is further amplified by oxidative stress and an

excess of proteases in the lung.

• Physiological changes characteristic of the disease include mucus

hypersecretion, air-flow limitation and air trapping (leading to

hyperinflation) , gas exchange abnormalities, and corpulmonale.(17)

• Systemic features of COPD, particularly in patients with severe

disease, include cachexia, skeletal muscle wasting, increased risk

of cardiovascular disease, anemia, osteoporosis, and depression.

• Exacerbations represent a further amplification in the airways of

patients with COPD, and may be triggered by infection with

bacteria or viruses or by environmental pollutants.

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OXIDATIVE STRESS:

Oxidative stress may be an important amplifying mechanism in

COPD. Biomarker of oxidative stress (e.g., hydrogen peroxide, 8-

isoprostane) are increased in the exhaled breath condensate, sputum, and

systemic circulation of COPD patients. Oxidative stress is further

increased in exacerbations. Oxidants are generated by cigarette smoke

and other inhaled particulates, and released from activated inflammatory

cells such as macrophages and neutrophils.

There may also be a reduction in endogenous antioxidants in

COPD patients. Oxidative stress has several adverse consequences in the

lungs, including activation of inflammatory genes, inactivation of

antiproteases, stimulation of mucus secretion, and stimulation of

increased plasma exudation. Many of these adverse effects are mediated

by peroxynitrite, which is formed via and interaction between protease-

non protease imbalance.

PROTEASE-ANTIPROTEASE IMBALANCE

There is compelling evidence for an imbalance in the lungs of

COPD patients between proteases that break down connective tissue

components and antiporteases that protect against this. Several proteases,

derived from inflammatory cells and epithelial cells, are increased in

COPD patients. There is increasing evidence that they may interact with

each other.(18)

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Protease-mediated destruction of elastin, a major connective tissue

component in lung parenchyma and is an important feature of

emphysema.

SYSTEMIC FEATURES

It is increasingly recognized that COPD involves several systemic

features, particularly in patients with severe disease, and that these have a

major impact on survival and comorbid diseases. Cachexia is commonly

seen in patients with severe COPD. There may be a loss of skeletal

muscle mass and weakness as a result of increased apoptosis and /or

muscle disuse.

Patients with COPD also have increased likeliness of having

osteoporosis, depression and chronic anemia. Increased concentrations of

inflammatory mediators, including TNF- �, IL-6 and oxygen-derived free

radicals, may mediate some of these systemic effects. There is an increase

in the risk of cardiovascular diseases, which is correlated with and

increase in C-reactive protein (CRP).(19)

EXACERBATIONS

Exacerbations represent a further amplification of the inflammatory

response in the airways of COPD patients, and may be triggered by

infection with bacteria or viruses or by environmental pollutants. There is

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a relative lack of information about the inflammatory mechanisms

involved in exacerbations of COPD. In mild and moderated exacerbations

there is an increase in neutrophils and in some studies also eosinophils in

sputum and the airway wall. This is associated with increased

concentrations of certain mediators, including TNF-�, LTB4 and IL-8,

and an increase in biomarkers of oxidative stress.

There is even less information about severe exacerbations,

although on study showed a marked increase in neutrophils in the airway

wall and increased expression of chemokines. During an exacerbation

there is increased hyperinflation and air trapping, with reduced expiratory

flow, thus accounting for the increased dyspnea. There is also worsening

of VA/Q abnormalities resulting in severe hypoxemia.(20)

PATHOLOGY:

Pathologic changes characteristic of COPD are found in the

proximal airways, peripheral airways, lung parenchyma and pulmonary

vasculature. The pathological changes include chronic inflammation with

increased numbers of specific inflammatory cell types in different parts of

the lung, and structural changes resulting from repeated injury and repair.

In general the inflammatory and structural changes in the airways

increase with disease severity and persist on smoking cessation.

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Pathological changes in COPD.

Proximal airways (trachea, bronchi> 2 mm internal diameter)

Inflammatory cell: increased Macrophages, CD8+ (Cytotoxic) T

lymphocytes, few neutrophils or eosinophils

Structural changes: increased Goblet cells. Enlarged submucosal glands

(both leading to mucus hypersecretion), squamous metaplasia of

epithelium

Peripheral airways (bronchioles<2mm internal diameter)

Inflammatory cells: increased Macrophages, T Lymphocytes

(CD8+>CD4+), B lymphocytes, lymphoid follicles, fibroblasts, few

neutrophils or eosinophils

Structural changes: Airway wall thickening, Peribronchial fibrosis,

luminal inflammatory exudates, airway narrowing (obstructive

bronchiolitis) increased inflammatory response and exudates correlated

with disease severity

Lung parenchyma (respiratory bronchioles and alveoli)

Inflammatory cells: increased Macrophages, CD8+ T lymphocytes

Structural Changes: Alveolar wall destruction, apoptosis of epithelial

and endothelial cells.

• Centrilobular emphysema: dilatation and destruction of respiratory

bronchioles; most commonly seen in smokers

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• Panacinar emphysema: destruction of alveolar sacs as well as

respiratory bronchioles; most commonly seen in alpha – 1 antitrypsin

deficiency

Pulmonary Vasculature

Inflammatory cells: increased Macrophages,T lymphocytes

Structural Changes: Thickening of intima, endothelial cell dysfunction,

smooth muscle cell proliferation leads to pulmonary hypertension.

Fig 2: Mechanisms of Small Airway Obstruction in COPD

Small airways are the major sites of airflow limitation. Small

airways show a variety of lesions narrowing their lumina, including

goblet cell hyperplasia, mucosal and submuosal inflammatory cell,

edema, peribronchial fibrosis, intra luminal mucus plugs and increased

smooth muscle.(21)

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In large cartilaginous airways chronic bronchitis in associated with

hypertrophy of sub mucosal mucus producing glands.

Quantitation of this anatomic change is known as Reid Index is

based on thickness of submucosal glands to that of bronchial wall.

In patients with chronic bronchitis it is 0.44 ± 0.09 otherwise

normally 0.52 ± 0.08. emphysema begins as an increase in the number of

and sizes of alveolar fenestrate and results in eventual destruction of

alveolar septae and their attachments to terminal and respirator

bronchioles.

With centriacinar emphysema the distension and destruction are

mainly limited to the respiratory bronchioles with relatively less change

peripherally in the acinus.

Panacinar emphysema involves both central and peripheral

portions of acinus.

PATHOGENESIS OF EMPHYSEMA:

Chronic exposure to cigarette smoker, fumes and dust may lead to

inflammatory cell recruitment within terminal air space of the lungs.

These cells release elastolytic proteinases that damage the extracellular

matrix of the lung.

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Inflammatory Cells in COPD

Neutrophils: increased in sputum of normal smokers. Further increase in

COPD and related to disease severity. Few neutrophils are seen in tissue.

They may be important in mucus hypersecretion and through release of

proteases.(22)

Macrophages: Greatly increased numbers are seen in airway lumen, lung

parenchyma, and bronchoalveolar lavage fluid. Derived from blood

monocytes that differentiate within lung tissue. Produce increased

inflammatory mediators and proteases in COPD patients in response to

cigarette smoke and may show defective phagocytosis.

T lymphocytes: Both CD4+ and CD8+ cells are increased in the airway

wall and lung parenchyma, with increased CD8+:CD4+ratio. Increased

CD8+T cells (Tc1)and Th1 cells which secrete interferon-� and express

the chemokine receptor CXCR3. CD8+ cells may be cytotoxic to alveolar

cells, contributing to their destruction.

B lymphocytes: increased in peripheral airways and within lymphoid

follicles, possibly as a response to chronic colonization and infection of

the airways.

Eosinophils: increased eosinophil proteins in sputum and increased

eosinohils in airway wall during exacerbations.

Epithelial cells: may be activated by cigarette smoke to produce

inflammatory mediators.

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Inflammatory Mediators Involved in COPD

Chemotactic factors:

Lipid mediators : e.g., leukotriene B4(LTB4 )attracts neutrophils and T

lymphocytes

Chemokines :e.g interleukin–8 (IL-8)attracts neutrophils and monocytes

Proinflammatory cytokines: e.g., tumor necrosis factor –� (TNF- �),

IL-1�, and IL-6 amplify the inflammatory process and may contribute to

some of the systemic effects of COPD

Growth factors: e.g., transforming growth factor- (TGF-) may induce

fibrosis in small airways.

Fig:3 Pathogenesis of Emphysema

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PATHOPHYSIOLOGY:

AIRFLOW LIMITATION:

The extent of inflammation, fibrosis, and luminal exudates in small

airways is correlated with the reduction in FEV1/FVC ratio, and probably

with the accelerated decline in FEVI characteristic of COPD. Airflow

limitation and increased airway resistance may be caused by loss of

elastic recoil during passive exhalation due to emphysema, by increased

collapsibility of small airways through loss of radial traction on airway or

to intrinsic narrowing of small airways

HYPERINFLATION :

The residual volume and the functional residual capacity (FRC) are

almost higher than normal. In addition prolongation of expiration is

associated with obstruction which would lead to dynamic increase in FRC

(dynamic hyperinflation)

Dynamic hyprerinflation contributes additionally to discomfort

associated with air flow obstruction by flattening the diaphragm fiber

length and a perpendicular insertion with the lower ribs.(23)

IMPAIRED GAS EXCHANGE:

Maldistribution of inspired air and blood flow is always present.

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When the mismatching is severe, impairment of gas exchange is

reflected in the abnormalities of arterial blood gases.

Small airway narrowing causes a decrease in ventilation of their

distal alveolar acini. When the alveolar capillaries remain intact, this

results in mismatch of ventilation and perfusion leading to mild or

moderate hypoxemia.

COPD IS A DISEASE OF SYSTEMIC INFLAMMATION:

Chronic obstructive pulmonary disease has classically been

considered to be an intrathoracic condition characterized by poorly

reversible airway obstruction.

However COPD has been recently recognized as a multicomponent

disorder, associated with systemic inflammation and extra pulmonary

manifestations.

It has now been well documented that the inflammation that

develops in the patient, does not confine to the lungs, but spills into the

systemic circulation through the pulmonary vessels and predispose almost

every organ system in the body with particular predilection to the heart,

as the heart is the first organ that receives all the blood from the

pulmonary vasculature

There is always a persistant low grade systemic inflammatory

response present in part of COPD patients.

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Various studies have shown enhanced levels of acute phase

proteins like C-Reactive Protein (CRP ) and pro inflammatory cytokines

such as TNF - ∝ and IL – 6 in many COPD patients.

Moreover, there has been a consistent strong association between

reduced lung function and systemic inflammation. Even increased

polymorphism have been shown in the inflammatory genes and there is

increasing interest in identifying a haplotype of inflammatory genes

which predisposes to systemic manifestation of COPD.

These inflammatory markers along with persistent hypoxia

increase the basal metabolism in the body leading to catabolic changes

such as reduced muscle mass, wasting of skeletal muscles and

diaphragmatic weakness.

Further the systemic inflammation also increase oxidative stress in

various other organs.

Up to 70% of COPD have underlying osteoporosis. There has also

been a strong association between depression and COPD. There is

emerging evidence indicating insulin resistance in some COPD. Patients

due to systemic inflammation.(24)

COPD has also been related to increased cardiovascular morbidity

and diabetes mellitus.

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FIG 4: Systemic Effects of COPD Inflammation

Hypoxemia results in peripheral nerve damage by harming the

vasonervosum. In the early stages of ischemia mechanisms to reduce

peripheral neuropathy are activated, but these become insufficient over

time and obvious neuropathy is inevitable in chronic hypoxemia.

It has been hypothesized that the abnormal brain stem auditory

potential and visual evoked potential findings are due to brain stem

hypoxia which increases with severity of COPD.

In addition to chronic hypoxemia and hyperapnia, other associated

factors in patients with COPD, including tobacco smoking, malnutrition,

and drugs used in COPD treatments like long acting inhaled B2 agonists,

inhaled anticholinergic agents, inhaled glucocorticoids &sustained release

of theophyline , may be possibly associated with neuropathy seen in

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COPD patients. Factors contributing to the development of pulmonary

artery hypertension in COPD patients.

(i) ABNORMAL BLOOD GAS TENSIONS:

HYPOXEMIA:

In COPD there in a negative correlation between oxygen saturation

of the blood and pulmonary artery pressure. Hypoxemia is known to be a

potent arteriolar constrictor in the pulmonary circulation. As the severity

of disease progresses in COPD there is more arterial desaturation

correlation with an increase in pulmonaryartery pressure.

Exacerbation of COPD with hypoxemia are associated with acute

worsening of pulmonary hypertension.

Pulmonary artery pressure (P.pa) can also increase acutely during

the episodes of hypoxemia that occur during rapid eye movement of sleep

and it has been suggested that recurrent nocturnal pulmonary

hypertension can result in pathologic changes in pulmonary vessels and

fixed hypertension.(25)

HYPERCAPNEA:

In patients with COPD there in positive correlation between arterial

CO2 pressure (paco2) and pulmonary artery pressure. The mechanism

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could be a change in lung mechanism due to hyperventilation induced by

hypercapnea or the potentiation of hypoxia pulmonary vaso constriction.

ACIDEMIA:

Hypoxia and acidemia act synergistically to produce pulmonary

vasoconstriction in patients with COPD. Thus for as given oxygen

saturation the mean pulmonary artery pressure is higher with increasing

arterial hydrogen concentration.

(ii) EFFECTS OF ABNORMAL PULMONARY MECHANICS

Changes in airway resistance may augment pulmonary vascular

resistance in pulmonary artery pressure, correlating with decrease in

FEV1.

(iii) EFFECTS OF INCREASED CARDIAC OUTPUT:

In patient with COPD (Vascular bed may be reduced) even small

increase in flow that occurs during exercise may increase pulmonary

artery pressure.

(iv) EFFECTS OF BLOOD VISCOSITY:

Polycythemia can develop secondary to chronic hypoxemia in

COPD patients, this contributes to blood viscosity which also adds up to

the pulmonary artery hypertension (PAH)

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(v) ROLE OF PULMONARY ENDOTHELIUM:

There is increasing evidence that endothelial dysfunction is an

underlying factor in development of pulmonary artery hypertension. This

may result in reduction in nitric oxide synthesis or release in response to

hypoxemia.

Thus the putative role of nitric oxide in preventing an excessive

rise in pulmonary vascular tone, as a result of stimuli such as hypoxemia,

may be lost in COPD.

It has also been suggested that nitric oxide may have an inhibitory

effect on cell proliferation in the pulmonary vessel walls that therefore

has a role in preventing the vascular remodeling that occurs in hypoxic

COPD. Circulating levels of endothelin have been found to be increased

in patients who have emphysema and pulmonary hypertension.

PATHOLOGY:

Changes in pulmonary circulation occurs characteristically in the

peripheral arteries in patients with COPD. An early increase in intimal

thickness in small pulmonary arteries that occur due to accumulation of

smooth muscles that are laid down longitudinally along the length of the

vessel. Hypertrophy in muscular pulmonary vessels, has also been

reported in patients of COPD who develop sustained pulmonary arterial

hypertension.

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Pulmonary thrombosis may also occur in patients with COPD that

may be secondary to peripheral airway inflammation.

Thus structural changes rather than simply hypoxia,

vasoconstriction is the major factor in the development of sustained

pulmonary hypertension in patients with COPD.(26)

CONSEQUENCES OF PULMONARY HYPERTENSION IN COPD

Chronic bronchitis and emphysema usually coexist

pathologically.Those patients with either predominant chronic bronchitis

or emphysema.

The blue and bloated type also known as type B or non fighters

was thought to characterize the bronchial type of disease.

These patients had hypoxemia, hypercapnea and secondary

polycythemia, they developed pulmonary hypertension relatively early in

the course of disease. Right ventricular hypertrophy or corpulmonale

ensure and repeated episodes of right heart failure occurred.(27)

In contrast the pink puffers variety also known as type A or fighter,

represent the emphysematous patients characterized by severe

breathlessness, but with preservation of blood gas values thus no

pulmonary hypertension, at least until the later stages of disease.

It was not known that the degree of mucous gland hypertrophy

indicative of chronic bronchitis was similar whatsoever the clinical

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pattern and that more than 50% of patients with blue & bloated clinical

pattern had severe emphysema.

COR PULMONALE:

Corpulmonle is defined as right ventricular hypertrophy and

dilation secondary to pulmonary hypertension caused by disease of the

lung parenchyma and / or pulmonary vasculature, unrealated to both sides

of heart, the prevalence of corpulmonale is also higher in patients with

hypacapnia, hypoxemia and polycythemia.

OEDEMA

There is increasing evidence that the oedema which develops late

in the course of the disease in patients with COPD may not be entirely

due to right ventricular failure.

The key factor leading to changes in salt and water balance in

patients with COPD is the development of hypoxemia and hypercapnia.

The most consistent factor in renal function in patients with hypoxic

COPD, particularly those with oedema is a reduction in renal blood flow.

Hypercapnia reduces renal blood flow through catecholamine

release and via a neuraly mediated action. Arginine vasopressin(AVP)

levels may be in-appropriately high in patients with COPD. There is also

evidence of activation of rennin – angiotensin – aldosterone axis. Thus a

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complex interaction between pulmonary haemodynamics and changes in

salt, water and hormonal. homeostatsis occurs in patients with hypoxia

and hypercapnic COPD leading to peripheral oedema.

CLINICAL FEATURES:

The characteristic symptoms of COPD are breathlessness on

exertion, mostly accompanied by wheeze and cough, which is often but

not invariably productive. Most patients have a smoking history of at

heart 20 pack years before symptoms develop, commonly in the fifth

decade.(28)

PHYSICAL SIGNS:

These are not specific to the disease and depend on degree of air

flow limitation and over inflation. In early disease the only abnormal

findings is wheeze on forced expiration and forced expiratory time

prolonged beyond 6 seconds with more advanced disease the breathing

pattern is characteristic with a prolonged expiratory phase.

Some patients adopting pursed lip breathing on expiration which

may reduce expiratory airway collapse. The use of accessory muscles of

respiration particularly sternomastoid is seen in advanced disease. These

patients adopt the position of leaning forward, supporting themselves

with their aims to fix the shoulder girdle and allowing the use of

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pectoralis and latissimusdorsi muscle to increase chest wall movement

(the tripod position).

In later stages the chest is often barrel shaped, an increased anterior

posterior diameter, horizontal ribs, prominence of the sternal angle and

wide subcostal angle. An inspiratory tracheal tug may be detected. The

horizontal position of diaphragm also acts to pull on the lower ribs during

inspiration (Hoovers sign)

On percussion there is decreased cardiac and hepatic dullness

indicating overinflation.

Breath sounds may have a prolonged expiratory phase or may be

uniformly diminished.

RADIOLOGY:

Chest X-ray

There are no specific features on plain chest X-ray for chronic bronchitis.

⇒ The features casually described are for emphysema, bronchial wall

thickening seen as parallel line opacities on plain chest X-Ray has

been described in chronic bronchitis

Radiographic signs for emphysema are

• Low flattened diaphragm : the border of the diaphragm in the

midclavicular line below the seventh rib

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• Height of patients lung being greater than 29.9cm

• An obtuse costophrenic angle

• Reduction in size and number of pulmonary vessels particularly in

periphery of lung.

• Heart shadow is vertical and narrow

• In lateral film increase in the retrosternal airspace.

COMPUTED TOMOGRAPHY

Has greater sensitivity and specificity than plain chest X-ray for

emphysema but is rarely necessary except for diagnosis for diagnosis of

bronchiectasis & evaluation of bullous lung disease.

GAS TRANSFER FOR CARBON MONOXIDE

Gas transfer for carbon monoxide values are below normal in many

patients with COPD

ARTERIAL BLOOD GAS ANALYSIS:

Measurement of arterial blood gas is essential in patients with

COPD to confirm the degree of hypoxemia and hypercapnia & in acute

exacerbation to determine the hydrogen ion concentration

Other tests : ∝�AT level

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Clinical assessment : early systolic click

Electrocardiography : Tall peaked P waves in lead II, III & AVF

P Value > 2.5mm.Rt axis deviation

MANAGEMENT OF COPD

NON PHARMACOLOGICAL MEASURES

1. Smoking cessation

2. Basic information about COPD

3. Self management skills(29)

Pharmacological measures:

(i) Nicotine replacement therapy

(ii) Use of bupropion (abstinence)

(iii) Bronchodilators

GLUCOCORTICOSTEROIDS:

Inhaled glucocorticoids are appropriate for symptomatic COPD

patients with an FEV1 < 50% predicted (stage III & IV)

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HOME OXYGEN THERAPY (HOT)

OTHER PHARMACOLOGIC TREATMENT:

⇒ ∝� Antitrypsin Augmentation therapy

ANTIBIOTICS: amoxicillin or cefixime (400mg once daily)

ANTIMUCOLYTIC AGENTS

DIURETIC THERAPY (OEDEMATOUS PATIENTS)

VACCINES: Influenza vaccines

SPIROMETRY

The most robust test of airflow limitation in patients with COPD.

Forced expiratory volume in one second (FEV1) is recommended as the

measurement of choice in COPD:

• FEV1 is reproducible & objective measurement

• It is simple and relatively quiet to measure and can be measured at all

stages of the disease.

• The expiratory maneuver records not only FEV1 but also FVC and

FEV1 / FVC ratio less than 70% is diagnostic of airway obstruction.

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FLOW VOLUME LOOPS:

Expiratory flow at 75% or 50% of vital capacity have been used as

a measure of airflow limitation .

x-axis = volume in liters

y-axis = flow in liters/sec

ABC = inspiratory part of the loop (oval)

ACD = expiratory part of the loop (triangular)

ABCD=muscle dependent part of the loop

DA= effort (muscle)independent part of the loop

AC = vital capacity

CD= peak expiratory flow (PEFR)

Fig 5: Flow Volume Loops

TIMED VITAL CAPACITY (TVC) OR FORCED VITAL

CAPACITY (FVC)

FVC is the maximum volume of air which can be breathed out as

‘forcefully’ and ‘rapidly’ as possible following as maximum inspiration.

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Thus TVC is exactly similar to VC except that there is a special stress on

rapid, forcible and complete exhalation.

COMPONENTS OF TVC (FVC):

(i) FEV1 (Forced Expiratory Volume in 1 sec), i.e., volume of FVC

expired in the first sec of exhalation. Normal: 80% of FVC.

(ii) FEV2 (Forced Expiratory Volume in 2 sec), i.e. volume of FVC

expired in the first two seconds of exhalation. Normal: 95% of

FVC.

(iii) FEV3 (Forced Expiratory Volume in 3 sec), i.e. volume of FVC

expired in the first three seconds of exhalation. Normal: 98-100%

of FVC.

Clinical Significance of TVC (FVC): To distinguish between

‘restrictive’ and ‘obstructive’ lung disorders.

REVERSIBILITY TO BRONCHODILATORS:

1. To help distinguish those patients with marked reversibility (at least

12% or 200ml of FEV1) who have underlying asthma.

2. To aid with future management.

3. The FEV1 after bronchodilator is the best predictor of survival.(30)

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It is usually recommended that the response to bronchodilator be

assessed either using repeated doses from metered dose inhaler or in the

nebulized route.

VISUAL EVOKED POTENTIALS:

Introduction: the visual evoked potential (VEP) is primarily a

relatively large, positive polarity have generated in the occipital cortex in

response to visual stimulation. It measures the conduction time of

neuronal activity from the retinal to the occipital cortex and is used

clinically as a measures of the integrity and function of that pathway. The

optic nerve in the primary structure examined the VEP is of large enough

voltage that can be seen occasionally on a routine EEG as an occipital

wave within the first 150ms after a single photic stimulus of primary

interest is the latency of the positive wave at approximately 100ms after

stimulation called P100 peak is usually easy to recognize and measure(31)

VARIABLES INFLUENCING VEP

AGE

Age has been reported to influence the latency of P100 at a rate of

2.5 ms/decade after fifth decade This has been attributed to age-related

changes in both retina and the rostral part of visual system The amplitude

of VEP remains reasonably stable in the adult life. In the first decade, the

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amplitude is higher and the mean amplitude is almost double of adult

value however, beyond 50 years, there is conflicting data. In infants and

young children, the P100 latency on large checks (30º) reaches the adult

value by 20 weeks whereas the latency on smaller checks takes 5-6 years

to reach the adult value. The maximum change occurs in the first year of

life

GENDER

The P100 latency is longer in adult males compared to females.

This has been attributed to larger head size and lower core body

temperature in males . In the age group below 19 years, P100 latency does

not vary with sex although a longer latency does not vary with sex

although a longer latency has been reported in girls. The mean

P100amplitude is greater in females compared to males. Although its basis

is unknown, hormornal differences have been suggested

EYE DOMINANCE

The P100 wave obtained by stimulating the dominant eye is shorter

and amplitude greater compared to the no dominant eye The amplitude of

transient VEPs from mid-occipital electrode ipsilateeral to hemi field

stimulation is greater in right hemi-field stimulation in right-handed

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individuals. This has been attributed to the neuro anatomic asymmetries

of human striate cortex

EYE MOVEMENT

Eye movement reduces the amplitude of P100, but its latency is not

affected .the patients with nystagmus having a normal visual pathway

also have normal P100 latency.

VISUAL ACUITY

P100 latency remains normal in spite of pronounced diminution of

visual acuity. The latency of P100 is reported to be normal with visual

acuity as low as 20/120; however, the amplitude decreases with further

reduction of visual acuity.

DRUGS

Drugs producing papillary constriction such as pilocarpine can

increase P100 latency, which is attributed to decreases area of retinal

illumination. The mydriatics result in an opposite effect.

REPRODUCIBILITY AND VARIABILITY

During mental activity such as problem solving, the P100 latency

has been reported to decrease and the amplitude increase. An

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unmotivated patient may alter the P100 latency or amplitude by closing

the eye, gazing off the screen, converging in front of target or even his

nose. These variables can often be detected by an observant technologist.

Simultaneous recording of Pattern electroretinogram (PERG) also helps

in documenting the fixation. An abnormal PERG raises the possibility of

improper fixation or retinal diseases; whereas a normal PERG suggests

adequate fixation. Whereas a normal PERG suggests adequate fixation.

Although the VEP waveforms are reproducible, they have an inherent

intraindividual variability. VEPs were repeated on three different

occasions within 1 week; P100 latency varied between 0 ms to 8 ms and

the inter-eye difference between 0ms and 6ms. In another study,

intraocular variability over a period of 6 months ranged up to 11 ms and

inter-eye variability up to 9ms. (32)

STEADY-STATE VEP

Steady –state VEPs are the response to visual stimuli given at a

rate of 3.5Hz or more. These responses overlap one another and appear as

somewhat sinusoidal oscillations, which persist during the period of

stimulation. Steady-state VEPs are also defined as repetitive evoked

potentials, which constitute discrete frequency components and remain

constant in amplitude and phase over an infinitely long period of time.

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BASIS OF VEP ABNORMALITIES

The eyes are tested on at a time and each eye projects to the

occipital cortex through the optic chiasma. The unilateral VEP

abnormality therefore, obtained by full field monocular stimulation is

likely to be due to prechiasmal lesion. It the PSVEP is abnormal

bilaterally, it is not possible to locate the anatomical site of conduction

defect in the visual pathways. The VEP abnormalities may be:

1. Latency prolongation

2. Amplitude reduction

3. Combined latency and amplitude abnormalities

The commonest cause of prolonged P100 latency is demyelination in

the optic pathways where the amplitude of P100 remains normal. Sparing

of the P100 amplitude in demyelination was investigated in a study by

giving paired stimuli. The interstimulus interval if less than 40ms, the

second stimulus was abolished by the first. This may be responsible for

the preservation of P100 amplitude as well as its shape in partial optic

nerve demyelination, where the late arriving impulses through

demyelinated segments are inhibited. The latency and shape of P100

depend upon the surviving fastest conducting fibres. It has been

calculated that a demyelinating plaque of 10mm size would result in VEP

delay of 25ms Care must be taken in interpreting the delay of P100

latency. The amplitude of P100 has a wide interindividual variation

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reducing its clinical utility. Intraocular amplitude ratio, therefore, has

been used for defining the abnormalities. Ischemic optic neuropathy

leading to axonal loss produces normal P100 latency and decreased

amplitude. The variables resulting in reduced retinal illumination such as

papillary size, refractive error, media opacities, and retinal diseases, etc.,

can lead to reduced amplitude. Optic nerve compression produces

segmental demyelination and axonal loss resulting in both latency and

amplitude abnormalities in VEP.

Shape abnormalities of P100 manifest with a W-shaped complex

(bifid pattern of P100) in which the two peaks are separated by 10-50ms.

This pattern is seen very rarely in normal individuals and its presence

usually suggests abnormality. The bifid P100 wave form may be attribute

to the following:

1. The upper visual field may contribute as negative polarity and

the lower as positive at inion. A summation of these tow

activates may result in W-shaped P100 waveform. This may be

excluded by recording the VEP by lower half visual field

stimulation

2. In patients with visual field defect, the “W” shape of VEP may

be due to shifting of transitional zone. This effect can be

eliminated by placing the recording electrodes laterally.

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COMPONENTS OF ELECTRO DIAGNOSTIC EQUIPMENT

Electrodes (Active, Reference & Ground)

ELECTRODES

(i) There are types of electrodes: active, reference and ground. The

action potential is measured between active and reference

electrode whereas the ground electrode serves as a ‘zero’

voltage reference point.

(ii) They are made up of platinum, stainless steel, silver chloride,

chromium, nickel, silver and gold. Silver or gold electrodes

have the advantage of stable electrode polarization potentials

which result in noise-free recording.

(iii) In clinical practice, two varieties of electrodes are used: surface

and needle electrodes. In general, surface electrode is preferred,

Analog

display Stimulator

Amplifie Filter

Analogue

to digital

converter

(ADC)

Micro-

processo

Video

monitor

Audio

monitor

Memory

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as using the needle electrodes have a greater chance of

infection.

(a) The surface electrodes are in the form of disc, cup or ring,

and are used in nerve conduction and motor evoked potential

recording. These electrodes are placed in position with the

help of electrode paste or jelly, which is gently rubbed on the

skin and then applied for proper contact.

(b) Needle electrode is commonly used for EMG study. They

consist of Teflon coated stainless steel wire which tapers to a

sharp tip.(33)

AMPLIFIER

A variable degree of amplification, up to 5x 105 folds is needed

before being displayed because of the following reasons:

(i) Biological signals are very small.

(ii) Intrinsic impedance of electrode. It varies with frequency and

electrode type used. The concentric needles have a higher

impedance.

(iii) Impedance of electrode-skin.

FILTER

It is a device that relatively allows a particular range of frequency

from a signal. It is required for eliminating the noise and useful for

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bringing out the characteristics of the waveforms, i.e. Optimising the

recording.

(i) The low- frequency filters remove the slowly changing low-

frequency (up to 100HZ) components and allow the higher

frequencies to pass through. Therefore, it is also called as high pass

filter.

(ii) The high-frequency filters remove the rapidly changing high-

frequency components and allow the low frequency (up to 100Hz)

to pass through; therefore, it is also called low pass filters.

AVERAGER

(i) It extracts very small signals which are hidden or buried in large

noise; for example:

(a) Evoked potentials are buried in EEC noise; and

(b) Sensory nerve action potential (SNAP) in EMG noise

(ii) By averaging, the time-locked signals become prominent and

are stored in the memory of the equipment, while the noise

which is occurring randomly is cancelled out. Alternatively, the

noise can be time-locked and can be rejected subsequently.

DISPLAY

Two methods of waveform display are in use:

(i) Analogue oscilloscope display; and

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(ii) Computer based digital video display

(i) Analogue Oscilloscope Display

Here the action potential signals are directly displayed on

cathode ray oscilloscope following amplification and filtering. It

can redisplay the waveform but certain details of waveform may

be lost.

(ii) Computer Based Digital Video Display

Here and analogue to digital converter (ADC) and digital

processing technique are used; therefore, the signals can be

redisplayed with greater sensitivity without any loss of

waveform accuracy.

STIMULATOR

It is required for nerve conduction and evoked potential studies.

Two types of stimulator are in use: Electrical and Magnetic.

(i) Electrical stimulators: It is of two types:

(a) Constant current stimulator: It delivers a constant current to

the subject over a wide range of stimulating electrode

impedance. Thus it is more stable and useful in repetitive nerve

stimulation and evoked potential studies.

(b) Constant voltage stimulator: It delivers a fixed voltage

between anode and cathode.

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(ii) Magnetic stimulators: they are used for the non-invasive

stimulation of motor cortex, spinal cord and peripheral nerves.

SENSITIVITY (OR GAIN) AND SWEEP SPEED

The latency and duration of an action potential is influenced by

sensitivity (i.e. gain) and sweep speed (or time).

(i) On high sensitivity, there is the shortening of latency due to the

visualization of smaller deflection from the base line.

(ii) Increase in sweep speed results in the shortening of latency.

SIGNAL TRIGGER

It is useful for isolating and displaying the action potentials for

their quantitative analysis. It can be fixed and time-locked relative to the

start to sweep.

DELAY TIME

It continuously samples and stores into the memory ongoing action

potential activities. The action potential when exceeds the triggering

values, it is extracted from the memory and displayed.

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LATENCY

• It is the time in msec from the stimulus artifact to the first negative

deflection of CMAP.

• It is a measure of conduction in the fastest conducting motor fibers.

• It includes neuro-muscular transmission time and propagation time

along the muscle membrane.(34)

AMPLITUDE

It is measured from baseline to the negative peak (base to peak) or

between negative and positive peaks (peak to peak).

Fig6: VEP in a normal individual

NORMAL VALUES FOR P100 V.E.P

(a) Latency : 100 msec.

(b) Amplitude : 10µV; and

(c) Duration : 60msec.

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APPLICATION:

• Prolonged latency of P100 – demyelination of optic pathway

• Amplitude reduction of N75-P100 amplitude – Axonal loss

• Combined latency and amplitude defects : optic nerve compression

BRAIN STEM AUDITORY EVOKED POTENTIAL (BAEP)

It was in 1967 Sohmer and Feinmesser published the first known

reported recording cochlear potentials using surface electrodes in

humans. It was only in 1971 Jewett and Williston gave clear description

of these. Waves and interpreted that the later waves were generated at the

level of brain stem.

In 1977 selters and Brackmandescribed the importance of

prolonged interpeak latencies in patients with acoustic tumors. They also

postulated that this time delay was directly proportional to the size of the

tumor.

In 1975 it was Starr and Achor reported the effects of ABR

(auditory brain stem response) in patients with pathology of in the brain

stem.

Even though BERA provides information regarding auditory

function and sensitivity. It should not be considered as a substitute for

other methods of audiological evaluations. More over ideally it should be

viewed in conjunction with other audiological investigations.

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This test involves recording of all forms of electrical response

generated at the level of brain. Stem in response to click/tone impulse by

placement of electrodes in the scalp. Stimulus is ideally provided by a

transducer placed in the insert earphone or head phone.

In auditory brain stem evoked response, the potentials are

generated by the brain stem. These recorded impulse contain a series of

peaks and troughs. The peaks are positive (vertex positive) and are

indicated by Roman Numerals I – VII.(35)

Normal BAEP, potential field distribution, waveform recognition,

and normal values

Classical BAEP consists of 5-8 vertex positive peaks, which are

labeled using Roman numerals. The initial five peaks are of clinical

interest. The succeeding peaks VI-VIII are quite variables and therefore

are not clinically useful. The through immediately following the peaks

are designated by the same numerical followed by a prime mark, e.g., the

trough of wave I is designated as I, the important features useful in the

recognition of different waveforms are as follows.

Wave I

Wave I is a prominent initial up – going peak in the ipsilateral ear-

recording channel. It appears 1.4 ms after the stimulus and is markedly

attenuated or absent from the contralateral ear-recording channel.

Employing a reference, wave I has a wide distribution of positivity and

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negativity. The later is confined to the ipsilateral ear. Medial earlobe

recording provides higher amplitude of wave I compared to mastoid In a

difficult case, the amplitude of wave I can be improved by following

maneuvers:

1. Horizontal montage

2. Use of external canal needle electrode

3. Use of nasopharyngeal electrode

4. Increasing the stimulus intensity

5. Decreasing the stimulus rate

6. Alternating click polarity to reduce the stimulus artifact

Patients with central nervous systems problems only, should have a

preserved wave I since it originates from VII nerve. Conversely, the

patients with significant peripheral hearing impairment may have a very

poorly formed or absent wave I but relatively normal wave II-V. wave I

sometimes may have two separate components. The earlier component is

of higher amplitude especially during high intensity and high pitch

simulation. This component should be used for measurement. The later

component is of lower amplitude and is recorded at a more wide range of

stimulus intensity and pitch.

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Wave II

Wave II is poorly defined in some adults and most neonates. It

sometimes appears as a small peak along the down – going slope of wave

I or in the up-going slope of wave III. It is more prominent in contra

lateral channel recording where it has a slightly prolonged latency

compared to ipsilateral. Absence of wave I on contralateral recording

may be helpful in differentiating wave I from wave II. Sometimes the

fusion of waves II and III results in M-shaped II-III complex.

Wave III

Wave III is usually a prominent peak, in the contralateral channel,

wave III often appears smaller and earlier than the ipsilateral ear because

its amplitude is similar at the vertex and contralarteral ear. This feature

may help in wave III recognition. Some normal subjects have a bifid

wave III, which is associated which is associated with a normal I-V IPL.

As with different configurations of wave IV and V, bifid wave III may be

related to the condensation or rarefaction clicks. In infants and some

adults, wave IV may normally be closer to III than to V and give and

appearance of bifid wave III. In contrast to wave IV and V, were II and

III tend to fuse in Ac-Cz recording , thus the latency of wave III

decreases and that of II increases. In some patients, a wave II-III complex

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forms in the Ac-Cz derivation. This may help in the recognition of these

waves.

Wave IV and V

Wave I is the most prominent peak appearing 5.5ms after the

stimulus. It starts above the baseline and its trough is maximal below the

base line. On ispsilateral recording wave V fuses with IV resulting in a

wave IV-V complex. The wave IV and V may have the following

patterns.

1. Single peak which is completely fused as a tall wide pyramid, whose

base should be more than 1.5ms

2. Two peaks which are close but sill visibly separated

3. Wave IV may be on the up-going slope of wave V

4. Wave V may be on the down – going slope of wave IV]

5. Wave I and V tend to be separated on contralateral recording.

For recognizing wave V the following maneuvers are helpful:

1. On reducing the click intensity to as low as 10dB, wave V is the last

wave to persist in that area.

2. On increasing the rate of stimulation to as high as 100Hz, wave V

persists but the earlier waves disappear.

3. On Ai-Ac montage, wave V amplitude decreases.

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Normal values of BAEP

Wave

(Latency ms)

Chiappa et al.

(1979)

Misra and Kalita

(n=30pts, 15-68

years)

I 1.7 ± 0.15 1.67±0.17

II 2.8 ± 0.17 2.78±0.21

III 3.9 ± 0.19 3.65±0.22

IV 5.1 ± 0.24 5.0±0.30

V 5.7±0.25 5.72±0.3

VI 7.3±0.29 7.2±0.48

I-III IPL 2.1±0.15 1.99±0.25

III-V IPL 1.9±0.18 2.08±0.30

I-V IPL 4.0±0.23 4.04±0.25

Fig 7:BAEP in a normal individual

The wave peaks have been postulated to arise from:

1. Cochlear nerves – Waves I and II

2. Cochlear nucleus – wave III

3. Superior olivary complex – wave IV

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4. Nucleus of lateral lemniscus – wave V

5. Inferior colliculus – wave VI and VII

APPLICATION:

• It is an effective screening tool for evaluating cases of deafness due to

retrocochlear pathology i.e (Acoustic schwannoma). An abnormal

BERA is an indication for MRI scan.

• Used in screening newborns for deafness

• Used for intraoperative monitoring of central and peripheral nervous

system

• Monitoring patients in intensive care units

• Diagnosing suspected demyelinating disorders.(36)

C REACTIVE PROTEIN (CRP) :

Also known as pentraxin 1, is a non-glycosylated protein in

pentraxin family that also includes pentraxin 2/SAP and pentraxin

3/TSG-14. CRP is an acute phase reactant, a protein made by the liver

and released into the blood within a few hours after tissue injury, the start

of an infection, or other cause of inflammation.

A high level of CRP in the blood is a sign that there may be an

inflammatory process occurring in the body.(37)

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MATERIALS AND METHODS

This case – control study was conducted at Thanjavur medical

college and hospital between February 2016-June 2017. It included 40

COPD patients recruited from chest outpatient clinic and 40 age and

matched as a control group. This study based on criteria defined in the

global initiative for chronic obstructive lung disease (gold) 2004

guidelines.

EXCLUSION CRITERIA: Patients with chronic neuropathy

without COPD, diabetes mellitus, chronic alcoholism, uremia, cystic

fibrosis, sarcoidosis, leprosy, malignancy, history of intake of neurotoxic

drugs, hearing and visual impairment.

Informed written consent from the study and control group

obtained

INCLUSION CRITERIA:cases were selected from COPD chest

outpatient clinic for regular follow. The patients were included only if

they had a stable course of disease with regular follow – up with no

hospitalization for COPD related illness during the preceding six months.

The diagnosis was based on the modified criteria defined in the Global

Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, and

had irreversible /partially reversible obstruction of airflow.

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PULMONARY FUNCTION TEST: were performed using

computerized spirometer (INTEX 17) digital suga monitor model No:17

– 173SB, spiroexcel – MEDICAID. The following indices were recorded

FVC, FEV1&FEV1/FVC.

VEP and BAEP: Was carried out using digital four channel polygraph

intex monitor, MRI GNAINI – 15”/17’ INSTUMENT MODEL IT -

173SB.

PULMONARY FUNCTION TEST(PFT) :

Recorded using computerized spirometry. These days

computerized multifunctional spirometers are available which allow high-

quality made virtually breath. These spirometers display to high-

resolution graphic display as well as the predicted curves. The generated

reports may be seen on the display or can be printed. All pulmonary

function test parameters with actual. Predicted and percentage predicted

values, as well as normal range with the option of interpretation and lung

age can also be obtained. Moreover, all tests performed are presented

with both the selected test highlighted and the percentage variation from

best.

The subject is made to sit comfortable in a stool facing the

spirometer, nose is clipped and the mouthpiece is inserted between the

teeth and the lips.

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The subject is then instructed to breathe in with maximum effort

form the end of resting expiration and subsequently to breathe out

completely with maximum effort. He is beforehand instructed not to

breathe in while he is breathing out. At least three such forced vital

capacity (FVC) curves are obtained and the maximum (best performance)

of three values is taken for calculation purposes, and other parameters

FEV1, FEV1/FVC etc. will be displayed with graphic display.

Fig 8: PFT demonstration

VEPs were recorded in a dark room 100cm away from the monitor.

A chess board pattern reversal method on a 12 inch screen. Stimulation

frequency at speed of 2Hz.

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STIMULUS: the standard stimulus for VEPs is a checker board

pattern in which the squares alternate from black to white – the pattern

reversal VEP (PRVEP) Dark squarer become light and vice versa,

without a change in the overall. Luminance of the display. Typically, the

pattern is reversed 100 or 128 times at 1 to 2 Hz, and the results are then

averaged. Usually a repeat trial of averaged stimuli & also recorded.

PRVEPS require maintaining visual fixation on the center of the

pattern. The occipital cortex is particularly sensitive to the perception of

edge and a sharp bordered checkerboard produces a strong and

measurable response. PRVEPs are remarkably precise and constant for a

given subject echo has no clinical change and are very sensitive to

dysfunction in the visual conducting system.

Check size: 8º x 8º for the entire stimulus or video screen

Contrast: contrast is the difference in luminance (or brightness) of the

dark and light areas divide by the sum of their luminances.

Repetition frequency: the pattern reversal rate is usually two per second.

Averaging: Voltage signals are averaged over 100 trials, usually with a

duration of 500-ms each. VEPs have a relatively high signal to noise

ratio, and a larger number of trails is not required.

Filter: The Low – frequency filter is usually set at 1 Hz and the high

frequency filter at 100 – 300 Hz. (The shape of the standard P100 has a

frequency of approx 15 - 20Hz)

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Fig 9: 10-20 Electrode placement system

VEP evaluation latency and amplitude P100 were assessed.

Sites where electrodes place were cleaned with 75% alcohol.

Electrodes were smeared with conductive paste, recording electrode was

positioned 1.5cm above the occipital bone reference on middle forehead,

ground electrode the vertex.

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Fig10 : VEP demonstration

BRAIN AUDITORY EVOKED POTENTIAL (BAEP)

PROCEDURE:

1. Keep the instrument out of view of the subject, allow the subject to

sit comfortable on a chair in a fully relaxed state, the skin at the

point of the placement of electrodes is cleaned with ether or spirit.

2. Using electrode paste, the recording (active) electrodes are placed

on both the ears, ipsilateral or mastoid process as per 10-20

international system of EEG electrode placement the reference

electrode is placed at the vertex, i.e. at Cz; the ground electrode is

placed at Fz.

3. Give a brief click stimulus which is usually a square wave pulse of

0.1 msec duration. A click rate of 11-31 Hz is most commonly

used in clinical practice.

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Were recorded in a quiet room at an intensity of 90dB, absolute

latencies of waves (I, II, III, IV& V) along with interpeak latencies

(IPLS) I-III, I-V & III-V.

Fig 11: BAEP demonstration

C – RP &BLOOD GLUCOSE: venous blood samplewere taken and

CRP were measured using semi automated analyzer - BIOSYSTEM 350

at siva clinical lab Thanjavur, by immunoturbido metric method (CRP)

and blood glucose by glucose oxidase method. (GOD)

PRINCIPLE OF CRP TEST:

The C-Reactive protein test is based on the principle of latex

agglutination. When latex particles complexed human anti-CRP are

mixed with a patients serum containing C-Reactive proteins, an visible

agglutination reaction will take place within 2 minutes. Normal C-

Reactive protein levels are below 3.0 mg/dl.

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RESULT

Statistics were done using spss version 21 by student ‘t’ test

method. We included 80 subjects comprising 40 COPD patient and age

matched 40 healthy subjects.

TABLE: 1 CHARACTERISTIC OF COPD PATIENTS GROUP

AND HEALTHY CONTROL GROUP

PARAMETRES

COPD

(n=40)

Mean ± SD

CONTROL

(n=40)

Mean ± SD

P-VALUE

Age 43.68 ± 7.8 42.88 ± 7.7 0.648

FEV1 (% of Predicted ) 58.15 ± 28.3 94.82 ± 26.9 0.0001*

FVC (% of Predicted) 63.6 ± 24.1 91.5 ± 25.3 0.0001*

FEV1/FVC (%) 96.77 ± 20.1 106.89 ± 7.4 0.004*

CRP (mg/ml) 2.01 ± 0.4 1.69 ± 0.3 0.001*

*Significant when P ≤ 0.05

The indices of spirometry of COPD patients were significantly

decreased from control. And CRP were significantly increased from

control. The serum level of C-reactive protein in COPD patients were

significantly elevated (Table.1)

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Diagram 1: ComparisionBetweenthe means of COPD and control of the

indices of – spirometry and CRP.

58.15

63.6

96.77

2.01

46

94.8291.5

99

1.69

16

0

10

20

30

40

50

60

70

80

90

100

FEV1 FVC FEV1/FVC CRP SMOKING

COPD

Ind

ices

o

fsp

iro

met

ry a

nd

CR

P

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TABLE:2 BRAIN – STEM AUDITORY EVOKED POTENTIALS

(BAEP) VARIABLES IN COPD PATIENTS AND CONTROL

GROUP

LEFT EAR

LATENCIES

COPD

(n=40)

Mean ± SD

CONTROL

(n=40)

Mean ± SD

P VALUE

I (ms) 2.19 ± 1.7 1.29 ± 0.9 0.0041*

II (ms) 2.91 ± 0.7 2.38 ± 1.1 0.016*

III (ms) 4.25 ± 0.8 3.49 ± 0.5 0.000*

IV (ms) 5.6 ± 1.1 4.9 ± 0.8 0.001*

V (ms) 6.8 ± 1.3 6.1 ± 1.1 0.012*

INTERPEAK

LATENCIES

COPD

(n=40)

Mean ± SD

CONTROL

(n=40)

Mean ± SD

P VALUE

I – III (ms) 2.47 ± 0.6 2.49 ± 0.8 0.905

III – V (ms) 2.6 ± 0.9 2.58 ± 0.9 0.730

I – V (ms) 5.27 ± 1.5 5.05 ± 1.1 0.474

* Significant P value < 0.05

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TABLE:3 BRAIN – STEM AUDITORY EVOKED POTENTIALS

(BAEP) VARIABLES IN COPD PATIENTS AND CONTROL

GROUP

RIGHT EAR

LATENCIES

COPD

(n=40)

Mean ± SD

CONTROL

(n=40)

Mean ± SD

P VALUE

I (ms) 1.67 ± 1.0 1.64 ± 3.2 0.956

II (ms) 2.78 ± 0.8 2.43 ± 1.4 0.189

III (ms) 4.01 ± 0.9 4.4 ± 7.0 0.670

IV (ms) 5.2 ± 1.0 5.8 ± 7.8 0.652

V (ms) 7.7 ± 6.6 6.6 ± 1.07 0.462

INTERPEAK

LATENCIES (IPLS)

COPD

(n=40)

CONTROL

(n=40) P VALUE

I – III (ms) 2.5± 0.7 2.39± 0.9 0.563

III – V (ms) 3.35± 4.1 2.39± 0.8 0.151

I – V (ms) 8.83± 10.2 6.8± 10.7 0.409

Significant when P ≤ 0.05

Over left ear, the latencies of wave I, II, III, IV and V were

increased in COPD patients (table 3) and it is statically not significant.

Over the right ear the latencies of waves I, II, III, IV and V were

increased in COPD patients not significant.

The interpeak latencies (IPL) of I-III, I-V and III-V were prolonged

in COPD on both left and right ears (Table 3)

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Diagram 2 : Comparison Between The Means Of COPD Patients &

Control Group Of The Brain Stem Auditory Evoked Potential Of

Left Ear

2.19

2.91

4.25

5.6

6.8

1.29

2.38

3.49

4.9

6.1

0

1

2

3

4

5

6

7

8

9

10

I II III IV V

COPD CONTROL

Wav

e la

ten

cy

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TABLE: 4 VISUAL EVOKED POTENTIALS (VEP) VARIABLES

INCOPD PATIENTS AND CONTROLS

LEFT EYE

COPD

(n=40)

Mean ± SD

CONTROL

(n=40)

Mean ± SD

P-VALUE

Latency P100 (ms) 106.89 ± 13.9 104.6 ± 14.4 0.921

Amplitude (mv) 8.79 ± 18.7 14.9 ± 30 0.272

RIGHT EYE

COPD

(n=40)

Mean ± SD

CONTROL

(n=40)

Mean ± SD

P-VALUE

Latency P100 (ms) 103.38 ± 16.2 93.38 ± 16.3 0.007*

Amplitude 10.6 ± 16.0 5.91 ± 5.1 0.080

*Significant when P ≤ 0.05

Over left eye, the latency (P100) and Amplitude were prolonged in

COPD patients. Over the right eye the latency (P100) were significantly

increased in COPD patients (P < 0.05) and amplitude of right eye not

significant.(table 4)

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Diagram 3:Comparison Between The Means Of COPD Patients & Control

Group Of The Brain Stem Antibody Evoked Potential Of Right Ear

1.67

2.78

4.01

5.2

7.7

1.64

2.43

4.4

5.8

6.6

0

1

2

3

4

5

6

7

8

9

10

I II III IV V

COPD CONTROL

Wav

e la

tency

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TABLE – 5 CORRELATION OF BRAIN STEM AUDITORY

EVOKED POTENTIAL (BAEP) VARIABLES RECORDED OVER

LEFT EAR WITH SPIROMETRY INDICES

LEFT EAR

LATENCIES

FEV1% of

pred

FVC% of

pred

FEV1/FVC%

pred

I r

p -0.118

0.469

0.015

0.925

-0.111

0.496

II r

p -0.183

0.259

-0.0234

0.147

-0.52

0.750

III r

p -0.62

0.705

-0.092

0.573

-0.075

0.646

IV r

p -0.097

0.553

-0.91

0.578

-1.02

0.531

V r

p -0.095

0.561

-0.41

0.803

-0.141

0.387

INTERPEAK LATENCIES(IPLs)

I – III r

p -0.044

0.789

-0.014

0.933

-1.68

0.300

III – V r

p -0.033

0.841

0.035

0.831

-0.084

0.605

I – V r

p - 0.55

0.738

0.029

0.858

-0.105

0.517

r - correlation value

Significant when P ≤ 0.05

BAER wave II, III, IV & V latency and I-III interpeak latency showed

negative correlation with FEV1, FVC and FEV1/FVC% of predicted

value and not significant over left ear in COPD patients.

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TABLE–6: CORRELATION OF BRAIN STEM AUDITORY

EVOKED POTENTIAL (BAEP) VARIABLES RECORDED OVER

RIGHT EAR WITH SPIROMETRY INDICES

RIGHT EAR

LATENCIES

FEV1% of

pred

FVC% of

pred

FEV1/FVC%

pred

I r

p 0.015

0.925 -0.107

0.511

0.167

0.302

II r

p 0.254

0.114 0.150

0.356

0.202

0.212

III r

p 0.078

0.631 0.041

0.804

-0.015

0.929

IV r

p -0.001

0.995 -0.052

0.749

-0.021

0.898

V r

p 0.0167

0.302 0.133

0.415

0.114

0.485

INTERPEAK LATENCIES

I – III r

p 0.134

0.410

0.142

0.384

-0.067

0.681

III – V r

p 0.148

0.24

0.025

0.879

-0.033

0.838

I – V r

p 0.233

0.148

0.235

0.144

0.085

0.603

r - correlation value

Significant when P ≤ 0.05

BAER wave IV latency showed negative correlation with FEV1, FVC

and FEV1/FVC% of predicted value and not significant over right ear in

COPD patients.

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TABLE – 7: CORRELATION OF VISUAL EVOKED POTENTIAL

(VEP) VARIABLES RECORDED OVER LEFT AND RIGHT EYE

WITH SPIROMETRY INDICES

LEFT EAR

LATENCIES

FEV1% of

pred

FVC% of

pred

FEV1/FVC%

pred

P100 (ms) r p 0.036

0.824

0.059

0.716

-0.001

0994

Amplitude (mv) r p -0.128

0.432

-0.074

0.651

-0.234

0.147

RIGHT EAR

LATENCIES

FEV1% of

pred

FVC% of

pred

FEV1/FVC%

pred

P100 (ms) Rp -0.096

0.557

-0.020

0.902

-0.063

0.695

Amplitude (mv) r p 0.038

0.814

0.009

0.956

0.042

0.799

r - correlation value

Significant when P ≤ 0.05

The correlation between the VEP variables and the characteristics

of COPD patients revealed that the latency P100 of Right ear were

correlated negatively with the spirometric indices and the amplitude of

Right ear were correlated positively and not significant with the

spirometric indices.

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DIAGRAM 4:SCARTTERED PLOT DIAGRAM SHOWING

CORRELATION BETWEEN VEP VARIABLE OF LEFT EYE.

Negative correlation between <P100 latency and FEV1/ FVC index.

90

95

100

105

110

0 20 40 60 80 100 120

LP

10

0

FEV1/FVC

LP 100 Linear (LP 100)

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DIAGRAM 5: SCARTTERED PLOT DIAGRAM SHOWING

CORRELATION BETWEEN VEP VARIABLE OF LEFT EYE.

Negative correlation between <P100 latency and FEV1 percent.

95

97

99

101

103

105

107

109

0 10 20 30 40 50 60 70 80 90 100

LP

10

0

FEV1 %

LP 100 Linear (LP 100)

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TABLE 8: CORRELATION OF PFT VARIABLES WITH CRP IN

COPD PATIENTS

PARAMETERS CRP

% Predicted FVC r

p

0.187

0.248

% Predicted FEV1 r

p

0.062

0.703

% Predicted FEV1/FVC r

p

– 0.095

0.560

r - correlation value

Correlation of indices of spirometry (% predicted FVC, FEV1,

FEV1/FVC) with C- reactive protein, FEV1/FVC in COPD patients

showed negative correlation with CRP and statistically not significant.

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TABLE – 9: CORRELATION OF BRAIN STEM AUDITORY

EVOKED POTENTIAL (BAEP) VARIABLES RECORDED OVER

LEFT AND RIGHT EAR WITH CRP

LEFT EAR

LATENCIES CRP

I r

p

-0.211

0.190

II r

p

-0.125

0.441

III r

p

0.054

0.739

IV r

p

0.214

0.185

V r

p

0.215

0.442

INTERPEAKLATENCIES

I – III r

p

0.327

0.040

III – V r

p

0.185

0.253

I – V r

p

0.275

0.086

RIGHT EAR

LATENCIES CRP

I r

p

– 0.142

0.383

II r

p

0.383

0.873

III r

p

0.089

0.584

IV r

p

0.241

0.133

V r

p

0.024

0.883

INTERPEAK LATENCIES

I – III r

p

0.239

0.138

III – V r

p

0.180

0.268

I – V r

p

0.000

1.000

r - correlation value

Significant when P ≤ 0.05

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Correlation of brain – stem auditory evoked potentials (BAEP)

variables with C-reactive protein on both ears, BAEP wave III, IV and V

of left ear and BAEP wave I,II, III, IV and V of right ear shows positive

correlation with CRP on both ears, not significant but the interpeak

latency of left ear I-III shows significant positive correlation with

CRP.(table 9)

Interpeak latency I-III, III-V and I-V of left ear and interpeak

latency I-III, III-V, and I-V of right ear shows positive correlation with

CRP on both ears(table 9)

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Diagram 6: Comparison Between The Means Of COPD Patients &

Control Group taking p(100) of both eyes(VEP)

104.6106.89

103.38

93.38

10

20

30

40

50

60

70

80

90

100

110

120

Left Eye Right Eye

COPD CONTROL

P1

00

L

aten

cy a

nd

A

pti

tud

e

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TABLE – 10: CORRELATION OF VISUAL EVOKED

POTENTIAL (VEP) VARIABLES RECORDED OVER LEFT AND

RIGHT EYE WITH CRP.

LEFT EYE

LATENCY CRP

P100 (ms) r

p

0.303

0.057

Amplitude (mv) r

p

– 0.90

0.579

RIGHT EYE

LATENCY CRP

P100(ms) r

p

0.231

0.152

Amplitude (mv) r

p

0.015

0.927

r- correlation value

Significant when P ≤ 0.05

Correlation of visual evoked potential (VEP) variable with C-

reactive protein of both eyes.

VEP have latency (P100) shows positive correlation with CRP on

both eyes on the other hand. Wave amplitude of left eye shows negative

correlation with CRP but not significant.

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82

DISCUSSION COPD is a multisystem disorder that is frequently associated with

significant extra pulmonary manifestations Gupta et al (38)

Although COPD affects the lung, it also produces significant

systemic consequences. The consequences can be detected clinically and

appear to be associated with the presence of systemic inflammatory

markers.

In our study we included stable COPD with no clinical evidence of

any neuropathy.

Our aim is to evaluate the brain stem auditory evoked potentials

and visual evoked potential abnormalities in stable COPD patient and its

correlation with C-reactive protein as a part of multisystem disorder

Indeed it is widely accepted that COPD patients with hypoxemia

have a higher mortality. Which is improved with oxygen therapy,

hypoxemia triggers oxidative stress and inflammation in COPD patients.

There is now sufficient evidence to support the presence of extra

pulmonary or systemic consequences of COPD that can be detected

clinically(39)

El- Kady et al found statically significant difference for all audio

logical measures between the control group and COPD.

The present study showed significant prolonged latency and

interpeak latencies with decrease in amplitude on both ears.

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83

Sohma et al demonstrated depression of the auditory nerve brain

stem evoked response as well as vestibular and visual evoked potentials

during severe hypoxemia in cats.

In addition to chronic hypoxemia and hypercapnia, often associated

factors in patients with COPD, including tobacco, smoking malnutrition

and drugs used in COPD treatment like long acting inhaled B2 agonists,

inhaled anticholinergic agents, inhaled glucocorticords and sustained

release through of theophyline, may be possibly associated with

neuropathy seen in COPD patients.

Although COPD affects the lung, it also produces significant

systemic consequences. The consequences can be detected clinically and

appear to be associated with the presence of systemic inflammatory

markers.

Gan and co-workers were the first to note the importance of high

CRP levels in COPD patients. They showed that CRP is elevated in

patient who actively smoked. Brockhuizen et al found that CRP was a

marker of impaired energy metabolism, functional capacity and distress

in 102 severe COPD patients. It is widely accepted that CRP levels

relates to the presence of airflow obstruction. In the present study CRP

were significantly increased from control. The serum level of C-reactive

protein in COPD patients were significantly elevated, which is similar to

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84

study done by Denise Rossato Silva et al, Marcelo Basso Gazzana et al

and Marli Maria Knorstet al.(40)

There is no sufficient evidence to support the presence of extra

pulmonary or systemic consequences of COPD that can be detected

clinically and that could also be measured by the determination of level of

increased systemic inflammatory markers. CRP is one of these markers

that could reflect the total systemic inflammation.

Friss et al detected prolongations in BAER wave V and interpeak

latency of III-V in preterm infants under hypercarbic state they speculated

that hypercarbia had a deleterious effect as neuronal function. IPL of

BAER III-V which represents the central portion of the auditory pathway

was significantly correlated with Paco2 and H2O3 and pH of the arterial

blood gas.

In the present study showed the latencies of wave I,II,III, IV and V

over left ear were prolonged in COPD patients and statistically

significant.

Over the right ear the latencies of wave I, II, III, IV and V

increased in COPD patients but not significant. The interpeak latencies

(IPL) of I-III, I-V and III-V were increased in COPD on both left and

right ears and not significant. The results of the present study agreed with

friss et al, shomer et al, Gupta et al (41)

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85

Spirometry only gives us the pattern of lung function abnormality

(FEV1, FVC, FEV1/FVC), spirometry does not tell us if this patient has

asthma or COPD. The diagnosis will depend on the patients clinical

presentation and the spirometry merely provides collaborative evidence.

The results of the present study showed the indices of spirometry

(FEV1, FVC, FEV1/FVC) were significantly decreased from control. The

present study agreed with thunhou ong.et al.

In VEP significant increase in N -75 latency in COPD patients may

be attributed to synaptic delay or altered neuronal processing in optic

nerve which in accordance with the suggestion of singh et al. The P100

latency is the most consistent one having least variable peak when

compared with N75 and N145. Since, N145 wave is generated from extra-

striate visual cortex.(42)

The result of present study showed the latency (P100) of left eye

were increased in COPD patients and Amplitude decreased in COPD

patients. Over the right eye the latency (P100) were significantly increased

in COPD patients (P<0.05) but amplitude of right eye not significant, this

finding is similar to the recent studies with oze et al.(43)

Sezer et al also showed that P100 value was altered in COPD patient

and further hypothesized that the elevations in latencies were brought

about by the hypoxia, hypercapnea and acidosis resulting from COPD.

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86

The finding of independency of factors viz. disease duration, smoking

and age on COPD corroborates with the observation of oze et al

In the present study showed in BAEP the latencies of wave I,II,III,

IV and V over left ear were prolonged in COPD patients and statistically

significant.

BAER wave IV latency showed negative correlation with

FEV1,FVC and FEV1/FVC % of predicted value and not significant over

right ear these results matched with that reported by Gupta et al and could

not find any correlation between BAEP parameters and indices of

pulmonary function test.

The present study the correlation between the VEP variables and

the spirometric indices revealed that the latency P100 of right ear were

correlated negatively with the spirometric indices and the amplitude of

right ear were correlated positively and not significant with the PFT,

However oze et al evaluated optic nerve involvement with severe COPD

and they observed VEP abnormalities which is similar to our study.

We could not find any correlation between the BAEP, VEP

parameters and pulmonary function test parameters, the poor correlation

in spite of significant BAEP, VEP abnormalities is probably due to the

narrow range of patients characteristic and pulmonary function

parameters in our patients as we included relatively stable patients during

the early course of COPD

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87

Correlation of brain- stem auditory evoked potential (BAEP)

variables with C-reactive protein on both ears, BAEP wave III IV and V

of left ear and BAEP wave I, II, III, IV and V of right ear shows positive

correlation with Correlation with CRP on both ears, and not significant

but the interpeak latency of left ear I-III shows significant positive

correlation with CRP.

Interpeak latency I-III, III-V and I-V of left ear and interpeak

latency I-III, III-V and I-V of right ear shows positive correlation with

CRP on both ears. Which agrees with the study done by NesrienShalabi

et al Mohmed Abdel El salam et al, Fatma Abbas et al.(44)

Correlation of VEP variable with C-reactive protein over both eyes

VEP latency (P100) shows positive correlation with CRP over both eyes

on the other hand wave amplitude of left eye shows negative correlation

with CRP and not significant and is similar to study done be oze et al.

Correlation of indices of spirometry (% predicted FVC, FEV1,

FEV1/FVC) with C-reactive protein, FEV1/FVC in COPD patients

showed negative correlation with CRP and statistically not significant and

similar to study done by Oze et al.(45)

In our study BAER wave II, III, IV and V latencies and I-III

interpeak latency showed negative correlation with spirometric indices

and not significant over left ear in COPD patients.

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88

In this study the COPD and control group were matched in age and

sex. CRP levels were significantly higher in COPD patients and indices

of spirometry (FEV/FVC) were decreased significantly in COPD patients.

In VEP the latency (P100) of left eye were increased in COPD patients and

Amplitude decreased in COPD patients. Over the right eye the latency

(P100) were significantly increased in COPD patients (P<0.05) and

amplitude of right eye not significant.

These data suggest that airways obstruction and long lasting COPD

resulting in hypoxemia, hypercapnia and respiratory acidosis which in

turn affect the ponto-medullary portion of the brain.

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89

CONCLUSION

• Smoking, airway obstruction and long lasting COPD leading to

hypoxemia, hypercapnia and respiratory acidosis which may affect the

ponto-medullary portion of the brain.

This study confirm that there were subclinical VEP and BAEP

impairment resulted from COPD illness, which were related to the

severity and disease duration.

• optic and auditory nerves are commonly affected in COPD which

represent an additional problem to physical effect of COPD , and of

course both will reflect more impairment in quality of life. So early

discovery and correction of these factors might decrease disabilities

and help in improvement of quality of life of COPD patients.

• The findings from this study indicate that impairment of VEP and

BAEP occurred in association with mild chronic respiratory

insufficiency. Therefore, the respiratory condition must be taken into

account when evaluating VEP and BAEP.

• We found that the levels of CRP in stable COPD were not different as

compared to control subjects. These results if confirmed in a larger

study, which also excludes patients with comorbidities related to

chronic inflammation, could contribute to a better understanding of

CRP concentrations in COPD patients.

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BIBLIOGRAPHY

1. Sharma S.K.. “Chronic obstructive lung disease” API text book of medicine,

Siddarth N. Shah, 2003, 7th editionChapter 6, Pg. 297.

2. William MacNee “Chronic Bronchitis and emphysema”. Crofton and

Douglass Respiratory Diseases Chapter 616, edited by Antony Seaton,

Douglas Seaton, fifth edition, Blackwell Sciences, Volume – 1, 650.

3. Suzanne Hurd, Ph.D. “The impact of COPD on lung health world wide,

epidemiology and incidence:,Chest, 2000. Vol. 117 : 1S – 4S.”

4. Benjamin Burrows, Richard H.Earle. “Course and prognosis of chronic

obstructive lung disease”, The New England Journal of Medicine 1669, Vol.

280 – 8, Pg. 297 – 404.

5. Pfeifer G, Kunze K, Bruch M,: Polyneuropathy associated with chronic

hypoxemia: Prevalence in patients with chronic obstructive pulmonary

disease. J Neurol 1990;237 : 230 – 3.

6. Sezer M, Yaman M, and Oruc S, Visual evoked potential changes in chronic

obstructive pulmonary disease. Eur J Gen Med 2007; 4(3) : 115 – 118.

7. Gupta PP, Sood S, and Atreja A,: Evaluation of brainstem auditory evoked

potentials in stable patients with chronic obstructive pulmonary disease. Ann

Thorac med 2008; 4:128 – 34.

8. Man SF, cornett JE, Anthonisen NR, C-reactive protein and mortality in mild

to moderate chronic obstructive pulmonary disease. 2004.pp.249-66.

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Age Sex

Wave

Latency

P100(ms)

Amptitude

(mv)

Wave

Latency

I

II III IVInter Peak

Latency VI -III III - V I - V

96.9 ± 3.6 7.8 ± 1.9 1.67 ± 0.17 2.78 ± 0.01 3.65 ± 0.22 5.6 ± 0.30 5.72 ± 0.3 1.99 ± 0.25 2.08 ± 0.30 4.04 ± 0.25

1 33 M63.5

115

4.72

8.32

1.35

1.35

2.3

2.3

3.3.

3.3

5.12

5.12

5.75

5.12

1.95

1.95

2.65

2.65

4.6

4.6

2 36 M106

100.5

0

0

1.08

1.82

2.08

1.85

322

2.98

4.12

4.38

6.68

3.38

2.14

1.86

2.46

2.38

4.6

4.32

3 33 M97

98

2.7

3.28

1.05

1.05

2

2

3.98

3.98

5.03

5.03

6.15

6.15

2.93

2.93

2.17

2.14

5.1

5.1

4 44 M95

97

3.28

2.7

1.05

1.08

2.08

1.48

4.58

3.28

6.2

4.5

7.72

5.38

3.53

2.2

3.34

2.3

6.87

4.5

5 45 M92.8

102

2.83

1.4

1.23

1.23

2.2

2.2

3.25

3.25

4.3

4.3

3.42

3.45

2.02

2.02

2.17

2.17

4.19

4.19

6 55 M92.5

102

2.83

14.77

1.18

1.23

2.82

2.22

3.8

4.2

4.35

5.48

5.18

6.6

2.62

2.97

1.28

2.4

3.9

5.37

7 51 M7.55

88.5

13

3

1.1

1.12

1.92

2

2.92

2.88

3.98

3.35

4.95

4.18

1.92

1.38

2.03

1.6

3.95

2.95

8 53 M90.5

11.2

3

3

1.42

0.35

2.38

11

3.65

2.28

4.82

4.82

5.72

7.85

2.23

1.9

2.27

4.87

4.8

6.77

9 33 M105

87

2.83

2.83

1.23

0.98

2.68

2.12

3.85

2.3

4.88

4.3

6.3

5.82

2.62

2.32

2.45

2.52

5.47

4.84

10 34 M95.8

73.5

10.6

6.7

1.9

0.05

2.72

1.88

3.8

2.7

5.08

3.8

6.1

4.35

1.68

1.65

2.52

1.64

4.2

6.3

11 44 M79

73.5

2.7

2.7

1.05

0.8

2.17

2.1

3.28

3.4

4.25

4.6

5.45

5.65

2.23

2.6

2.17

2.25

4.4

4.85

12 47 F70

73.5

12

12.7

1.15

0.82

2.02

1.88

3.7

2.95

6.55

3.8

7.38

4.82

2.55

2.13

3.65

1.87

6.23

4.01

13 46 M88

79

1.12

2

0.68

0.68

1.7

1.7

2.78

2.78

4.42

4.42

6.05

6.05

2.1

2.1

3.3

3.3

5.4

5.4

CONTROL

Sl.

No

VEP FINDINGS BAEP FINDINGS

Page 101: EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC …repository-tnmgrmu.ac.in/9273/2/200500518anitcheady.pdf · blood viscosity and pulmonary vascular resistance which result in cor

Age Sex

Wave

Latency

P100(ms)

Amptitude

(mv)

Wave

Latency

I

II III IVInter Peak

Latency VI -III III - V I - V

Sl.

No

VEP FINDINGS BAEP FINDINGS

14 31 M86.8

74.8

15

1

1

1.2

1.92

2

2.92

2.58

3.98

3.35

4.95

4.18

1.92

1.38

2.03

1.6

3.95

2.98

15 33 M98

98

17.5

17.37

1.05

0.8

2.18

2.1

3.28

3.4

4.25

4.6

5.45

5.65

2.23

2.6

2.17

2.25

4.4

4.85

16 46 F103.5

103.5

6.94

6.94

1.08

0.75

1.92

1.55

2.98

2.78

5.08

3.82

6.98

49

1.9

1.9

4

4

5.9

5.9

17 44 M100.5

99

12.65

14.61

1

1.3

2

2.17

3.02

4.47

4.35

5.52

5.22

8.12

2.12

3.17

2.2

3.65

4.22

6.82

18 48 F107

97

9.43

10.21

6.78

0.82

1.7

1.88

2.68

2.8

4.05

4.25

6.72

5.52

1.9

1.9

4.04

2.7

3.94

4.7

19 49 M98

94

8.86

11.27

0.75

0.88

1.7

2.17

3.18

3.18

4.15

4.1

5.75

5.25

2.61

2.3

2.6

2.07

5.2

4.37

20 33 M102.5

101

18.7

19.42

0.55

0.65

2.3

2.5

3.08

4.7

7.05

5.15

8.05

5.92

6.5

4.05

0.53

1.22

6.5

5.27

21 37 M94.5

94.5

2.49

2.52

0.62

0.08

1.75

1.88

2.75

2.78

3.9

4.38

4.98

0.08

2.13

2.8

2.03

2.034.16

22 34 M100.5

99.5

8.05

7.71

1.18

1.08

2.2

2.08

4.4

3.22

5.72

5.05

7.88

7.88

2.2

2.14

3.48

4.63

6.7

6.77

23 51 F103.5

102

2.24

2.17

0.38

0.9

1.88

2.68

3.35

4.15

5.62

5.7

7.8

7.7

3

3.25

4.4

3.6

74

68.5

24 49 M102

107

8.55

7.3

0.98

1.3

2.9

2.62

4.28

4.88

5.78

5.7

7.2

6.82

3.3

3.55

2.92

1.74

6.22

3.32

25 47 M88

97

7.52

7.89

1.1

1.8

2.5

1.9

4

2.75

4.6

4.55

5.38

5.5

2.9

1.2

1.38

2.75

4.28

3.95

26 34 M104

104

7.01

1.1

1.98

2.2

2.78

2.9

3.4

48

4.05

6.3

5.03

6.85

1.42

2.63

1.63

2

3.08

4.63

27 36 M93.5

95.5

9.18

1.9

1.98

1.65

2.8

2.28

3.8

2.9

5.5

3.48

6.3

4.2

1.9

1.25

2.42

1.3

4.32

2.55

28 42 M100

100

5.8

8.7

0.95

1.58

2.45

2.58

2.88

4.15

3.72

4.88

6.42

5.6

1.93

5.75

3.54

1.45

5.47

4.02

29 44 F92.5

95.5

1.5

1.7

1.72

1.78

2.4

2.38

3.12

2.03

4.4

4.3

6

4.95

1.4

1.27

28

1.9

4.28

3.17

Page 102: EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC …repository-tnmgrmu.ac.in/9273/2/200500518anitcheady.pdf · blood viscosity and pulmonary vascular resistance which result in cor

Age Sex

Wave

Latency

P100(ms)

Amptitude

(mv)

I II III IV V I-III III-V I-V

96.9 ± 3.6 7.8 ± 1.9 1.67 ±0.17 2.78±0.21 3.65±0.22 5.6±0.30 5.72±0.3 1.99±0.25 2.08±0.30 4.04±0.25

41 51 M44.5

44.5

2.5

2.5

1.1

1.1

2.3

2.3

3.22

3.22

3.95

3.95

4.72

4.72

2.12

2.12

1.5

1.5

3.62

3.62

42 55 M 99.5

94.5

2.19

2.19

0.62

1.7

1.38

3.42

2.15

4.58

2.8

5.65

3.85

8.98

1.53

2.88

1.7

4.4

3.23

7.28

43 56 M109.5

109.5

4.9

4.9

1.95

1.95

2.88

2.88

3.85

3.85

5.52

5.52

6.38

6.38

1.9

1.9

2.5

2.5

4.4

4.4

44 31 M 100.5

102

7.31

16.22

0.78

1.05

1.95

2.65

4.03

3.7

7.55

5.08

8.85

7.55

3.25

3.25

4.82

3.85

8.07

6.5

45 32 M116

101

4.57

6.2

2.83

2.83

3.65

3.65

5.28

5.28

6.32

6.32

8.48

8.48

2.9

2.9

3.2

3.2

6.1

6.1

46 31 M 111

99

7.7

3.1

1.42

0.38

2.58

1.1

3.65

2.28

4.82

4.22

5.92

7.15

2.23

1.9

2.27

4.87

4.5

6.77

47 53 M103

112.5

13.1

23.3

1.23

0.98

2.68

2.12

3.85

3.3

4.88

4.53

6.3

5.82

2.62

2.32

2.45

2.52

5.07

4.84

48 44 F103

103

6.14

6.16

1.9

1.05

2.72

1.88

3.58

2.7

5.08

3.5

6.1

4.35

1.68

1.65

2.52

1.65

42

33

49 47 M102

103.8 123

1.82

1.82

3.08

3.08

4.03

4.03

5.3

5.3

6.32

6.32

2.21

2.21

2.29

2.29

4.5

4.5

50 51 M104

103.5

4

12

298

1

4

2.55

5.85

3.52

6.9

5.12

7.8

6.7

2.87

2.52

1.98

3.18

4.82

5.7

51 53 F109

106.5

1.7

6.51

1.62

1.32

2.33

4.03

3.42

5.03

4.58

6

5.6

8.22

1.8

3.71

2.18

3.19

3.98

6.9

52 57 M103

103.5

4.67

6.01

1.4

0.3

2.65

1.75

4.7

3.75

6.88

6.28

5.9

8.3

3.3

3.43

2.15

4.55

5.48

7.98

COPD (STUDY GROUP)

Sl.

No

BAEP FINDINGS

Wave Latency Inter Peak Latency VEP FINDINGS

Page 103: EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC …repository-tnmgrmu.ac.in/9273/2/200500518anitcheady.pdf · blood viscosity and pulmonary vascular resistance which result in cor

Age Sex

Wave

Latency

P100(ms)

Amptitude

(mv)

I II III IV V I-III III-V I-V

Sl.

No

BAEP FINDINGS

Wave Latency Inter Peak Latency VEP FINDINGS

53 41 M109.8

105

4.01

8.81

1.92

1.55

3.7

3.02

4.82

3.9

6.62

6.18

6.95

8.4

2.1

2.35

2.13

4.8

5.03

6.85

54 51 F104.5

104.5

7.86

7.86

1.27

1.88

3.05

2.68

4.75

5.83

7.08

6.05

9.65

7.05

3.48

3.48

4.9

2.02

8.38

8.47

55 32 M103.5

104.5

7.74

7.32

1.15

1.75

2.28

3.98

4.68

6.12

6.52

8.22

7.85

9.78

3.5

4.37

32

3.66

6.7

8.03

56 33 M102.5

98

4.93

4.01

4.03

4.03

5.32

5.32

6.1

6.1

7.55

7.55

8.38

8.38

2.07

2.07

2.28

2.28

4.35

43

57 34 M102.8

145

4.93

8.8

10.6

1.45

2.5

2.95

4.47

4.18

6.82

5.08

8.75

6.1

2.46

2

4.28

1.92

8.15

4.65

58 38 M104.5

99.5

7.64

1.9

1.32

1.9

2.08

3.02

3.78

3.9

4.75

3.32

6.4

6.7

2.46

2

2.62

28

5.8

4.8

59 57 F105.5

103

10.62

11.79

2.88

1.1

2.05

3.4

3.12

4.3

4.02

5.7

5.45

6.38

2.24

3.2

2.33

2.28

4.57

5.45

60 42 M103

102

6.17

5.54

1.08

2

2.58

2.88

4.08

3.35

5.5

4.12

5.85

6.2

3.03

1.35

1.8

2.85

4.83

42

61 41 M100

101

9.65

9.09

0.88

0.4

2.78

1.4

4.25

3.68

6.4

4.3

8.62

6.28

3.7

2.68

4.37

3.2

8.07

5.88

62 32 M103.5

108

7.64

6.36

1.25

1.45

2.9

2.92

4.4

4.15

5.82

5.95

7.32

7.48

3.15

2.7

2.92

3.33

6.07

6.03

63 41 M100

102

10.72

11.69

0.92

1

1.65

1.9

3.18

2.68

5.82

3.32

7.8

5.4

2.26

1.68

4.5

2.72

6.76

4.4

64 53 M103

103

7.88

7.58

2.4

1.88

3.9

3.72

5.18

4.55

6.55

5.6

7.88

7.7

2.67

2.67

3.15

3.15

8.82

8.82

65 48 F106

109

9.27

12.37

6.98

1.3

2.9

2.6

4.28

4.8

5.78

5.58

7.2

6.62

3.3

3.88

2.92

1.74

6.22

5.32

66 41 F 96 7.821.88

1.38

2.68

2.28

3.92

3.25

4.5

4.12

5.4

5.05

2.04

1.87

1.48

1.8

352

3.67

67 44 M102

100

8.3

15.61

1.82

6.98

2.88

2.48

3.22

3.32

4.18

4.53

4.9

5.85

1.4

2.34

1.68

2.53

3.08

4.87

Page 104: EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC …repository-tnmgrmu.ac.in/9273/2/200500518anitcheady.pdf · blood viscosity and pulmonary vascular resistance which result in cor

Age Sex

Wave

Latency

P100(ms)

Amptitude

(mv)

I II III IV V I-III III-V I-V

Sl.

No

BAEP FINDINGS

Wave Latency Inter Peak Latency VEP FINDINGS

68 45 M102

94

1.63

4

1.75

1.5

2.95

2.48

4

3.1

4.97

3.62

6

4.8

2.25

1.6

2

1.08

4.25

2.68

69 33 M101.5

89

7.86

1.54

1.18

1.12

24

1.85

3.48

3.62

4.58

4.95

5.2

5.45

2.3

2.5

1.72

1.83

4.02

4.33

70 33 M102.5

99.5

3.16

0.8

2.3

1.23

2.8

2

3.62

3.35

4.4

4.32

6.48

48

1.32

2.29

2.86

1.28

4.18

3.52

71 41 F97.5

93

5.35

72

2.3

1

3.32

2.1

4.28

2.8

5.03

4.88

5.82

6.02

1.98

1.8

1.59

3.22

3.52

5.02

72 47 F107

93

2.51

0.77

2.08

2.2

3.8

3.15

4.53

4.25

6.95

6.12

9.43

7.35

2.45

2.05

4.9

3.1

7.35

5.15

73 41 F107.8

110

4.04

0.39

1.25

1.45

2.9

2.9

4.4

4.15

5.82

5.95

7.32

7.48

3.15

2.7

2.92

3.33

6.07

6.03

74 43 M108

108

3.42

0.8

2.08

1.8

3.1

2.48

4.38

4.97

6.22

6.4

7.6

7.6

2.3

3.17

3.22

2.63

5.52

5.8

75 44 M111

104

4.85

0.93

1.9

1.2

2.8

2.37

4.88

3.7

6.58

5.55

7.82

6.68

2.98

2.45

2.94

2.98

5.92

5.43

Rt 43 M104

109

5.18

0.47

2.4

1.88

3.9

3.72

5.18

4.55

6.85

5.6

7.85

7.7

2.78

2.67

2.67

3.15

5.4

5.2

77 44 F106

106

3.63

2.72

1.68

1.25

2.5

3.38

5.22

4.38

6.8

5.9

7.1

6.03

3.54

3.05

1.88

1.6

5.42

4.65

78 47 F100

103

4.06

0.56

2.3

2.12

3.2

3

3.98

5.2

5.35

5.95

5.98

7.12

1.68

3.08

2

1.92

3.68

5

79 48 F113

97

4.34

8.54

2.92

1.98

3.32

1.95

5

2.78

5.78

4.42

6.7

4.75

2.08

1.7

1.7

1.97

3.78

3.6

80 49 M106.8

94

7.52

73

3.45

2.75

4.1

3.9

5.3

4.22

5.95

5.95

6.98

6.45

1.85

1.57

1.68

2.13

3.53

37

Page 105: EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC …repository-tnmgrmu.ac.in/9273/2/200500518anitcheady.pdf · blood viscosity and pulmonary vascular resistance which result in cor

CRPBlood

GlucosePredicted Measured % Predicted Predicted Measured

%

PredictedPredicted Measured % Predicted

<6mg/L 80-120mg FVC FVC FVC FEV1 FEV1 FEV1 FEV1/FVC FEV1/FVC FEV1/FVC

41 51 M S 1.2 83 4.28 1.98 46 3.62 1.83 51 81.09 92.12 114

42 55 M S 2.3 117 3.04 1.55 51.1 2.63 1.46 56 83.21 94.19 113

43 56 M S 2.8 118 4.07 1.92 47 3.49 1.35 39 81.63 70.31 86

44 31 M N 2.7 121 3.93 4.17 106 3.44 3.94 115 85.49 44.48 118

45 32 M N 2.6 126 4.48 3.62 81 3.88 2.81 72 83.25 47.62 93

46 31 M N 2.8 121 4.61 4.48 97 4.01 1.02 25 83.79 22.77 27

47 53 M N 1.9 75 4.67 2.08 48 4.05 1.95 48 83.79 93.78 112

48 44 F N 1.3 83 4.7 2.39 51 4.08 1.41 35 83.97 59 70

49 47 M N 1.7 87 4.7 2.39 51 4.08 1.41 35 83.97 59 70

50 51 M S 2.2 89 4.23 1.7 40 3.6 0.89 24 82.71 52.35 63

51 53 F N 2.3 91 4.25 5.81 137 3.61 5.4 116 82.89 92.94 112

52 57 M N 3.1 75 4.49 3.09 69 3.85 2.88 78 82.53 93.2 113

53 41 M N 2.8 103 3.57 0.37 10 3.12 0.37 12 84.54 110 118

54 51 F N 2.3 107 4.7 2.39 51 4.08 1.41 35 83.97 59 70

55 32 M S 2.3 109 4.23 1.7 40 3.6 0.89 24 82.71 52.35 63

56 33 M S 1.9 111 2.92 2.66 91 2.52 2.33 92 83.02 87.59 106

57 34 M S 1.8 108 3.91 1.37 65 3.32 0.014 28 80.55 68.61 85

58 38 M S 2.1 98 3.96 4.01 101 3.48 3.7 106 82.89 92.77 111

59 57 F N 2.1 81 4.33 4.15 96 3.75 3.78 110 83.43 91.08 109

60 42 M N 2.3 73 3.75 1.74 46 3.28 1.25 35 84.54 71.84 88

COPD(STUDY GROUP)

Sl.No

BLOOD TEST SPIROMETRIC INDICES

AGE SexSmok

ing

Page 106: EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC …repository-tnmgrmu.ac.in/9273/2/200500518anitcheady.pdf · blood viscosity and pulmonary vascular resistance which result in cor

CRPBlood

GlucosePredicted Measured % Predicted Predicted Measured

%

PredictedPredicted Measured % Predicted

<6mg/L 80-120mg FVC FVC FVC FEV1 FEV1 FEV1 FEV1/FVC FEV1/FVC FEV1/FVC

Sl.No

BLOOD TEST SPIROMETRIC INDICES

AGE SexSmok

ing

61 41 M N 2.4 84 3.75 1.74 46 3.28 1.25 25 84.54 71.84 85

62 32 M N 2 81 4.3 3.15 73 3.75 2.87 77 83.25 91.11 109

63 41 M S 1.9 83 3.75 2.58 69 3.35 2.22 66 83.43 86.05 103

64 53 M S 2.1 101 3.89 3.05 78 3.39 2.83 83 82.35 92.79 113

65 48 F N 1.7 121 3.01 1.74 58 2.6 1.17 45 82.07 67.24 82

66 41 F N 1.8 123 27 1.86 69 2.33 1.64 70 83.02 88.17 106

67 44 M N 1.9 123 3.4 1.55 46 2.97 1.41 47 84.92 90.77 107

68 45 M S 2 128 4.1 2.41 59 3.52 2.12 60 81.81 87.97 108

69 33 M S 1.7 129 4.36 3.25 75 3.81 2.77 73 83.61 85.23 102

70 33 M S 1.8 89 3.24 2.66 82 2.8 2.4 87 82.07 91.73 112

71 41 F N 1.9 98 3.85 1.74 48 3.37 1.16 34 84.92 66.67 79

72 47 F N 1.8 97 3.31 1.21 37 2.87 1.04 36 82.64 85.95 104

73 41 F S 2 96 3.31 1.82 55 2.87 1.58 55 82.64 86.81 103

74 43 M S 1.9 81 2.53 1.41 56 2.2 1.09 50 84.47 77.3 92

75 44 M S 1.7 83 4.3 3 70 3.75 2.97 79 83.25 99 119

76 43 M N 1.4 75 3.91 1.37 35 3.32 0.94 28 80.55 68.61 85

77 44 F N 2.1 81 2.92 2.66 91 2.52 2.33 92 83.02 87.59 100

78 47 F N 1 86 3.91 1.37 35 3.32 0.94 28 80.55 68.61 85

79 48 F N 1 87 4.3 3 70 3.75 2.97 79 83.25 99 119

80 49 M N 2 98 4.2 2.84 68 3.69 2.55 76 82.53 96.83 117

Page 107: EVALUATION OF VESTIBULOCOCHLEAR NERVE AND OPTIC …repository-tnmgrmu.ac.in/9273/2/200500518anitcheady.pdf · blood viscosity and pulmonary vascular resistance which result in cor

CRPBlood

GlucosePredicted Measured

%

PredictedPredicted Measured

%

PredictedPredicted Measured % Predicted

<6mg/L 80-120mg FVC FVC FVC FEV1 FEV1 FEV1 FEV1/FVC FEV1/FVC FEV1/FVC

1 33 M N 2.3 86 3.69 2.31 63 3.22 1.76 55 84.73 76.19 90

2 36 M N 1.2 73 3.93 4.17 106 3.44 3.94 115 85.49 94.48 111

3 33 M N 1.3 82 4.21 4.23 100 3.61 3.74 104 84.47 88.42 105

4 44 M N 1.1 61 2.96 3.13 106 2.71 2.97 101 84.47 94.89 112

5 45 M N 1.3 102 4.49 3.09 69 3.85 2.88 75 82.53 93.2 113

6 55 M N 1.2 101 4.49 3.09 69 3.85 2.88 78 82.53 93.2 113

7 51 M S 1.3 102 4.64 6.07 131 4.02 5.55 138 83.61 91.43 109

8 53 M N 1.8 101 4.3 3 70 3.78 2.97 79 83.75 99 119

9 33 M N 1.7 107 4.64 6.07 131 4.02 5.55 138 83.61 91.43 109

10 34 M N 1.6 86 4.35 3.25 81 3.86 2.86 82 82.35 88 107

11 44 M N 2.1 76 4.36 3.25 75 3.81 2.77 73 83.61 85.23 102

12 47 F N 2.9 71 4.33 3.35 77 3.78 3.06 81 83.43 91.34 109

13 46 M N 1.3 84 2.95 2.82 96 2.55 2.5 98 83.21 88.65 107

14 31 M N 1.7 113 4.64 6.07 131 4.02 5.55 138 83.61 91.43 109

15 33 M S 1.7 115 2.95 2.82 96 2.55 2.5 98 83.21 88.65 107

16 46 F N 1.9 116 4.36 3.28 78 3.81 2.77 73 83.61 85.23 102

17 44 M N 1.2 87 2.95 2.82 96 2.55 2.5 98 83.21 88.65 107

18 48 F N 2.1 88 3.29 2.66 81 2.88 2.59 90 85.68 97.37 114

19 49 M S 2.1 81 3.75 1.74 46 3.28 1.25 58 84.54 71.84 85

20 33 M N 1.1 98 4.64 6.07 131 4.02 5.55 135 83.61 91.43 109

CONTROL

Sl.

No

BLOOD TEST SPIROMETRIC INDICES

Age SexSmoki

ng

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CRPBlood

GlucosePredicted Measured

%

PredictedPredicted Measured

%

PredictedPredicted Measured % Predicted

<6mg/L 80-120mg FVC FVC FVC FEV1 FEV1 FEV1 FEV1/FVC FEV1/FVC FEV1/FVC

Sl.

No

BLOOD TEST SPIROMETRIC INDICES

Age SexSmoki

ng

21 37 M N 1.9 101 4.64 6.07 131 4.02 5.55 135 83.61 91.43 109

22 34 M N 1.7 82 4.2 2.84 60 3.6 2.75 76 82.53 96.83 117

23 51 F N 1.8 87 4.64 6.07 131 4.02 5.55 138 83.61 91.43 109

24 49 M N 1.7 73 3.69 2.31 63 3.22 1.76 55 84.73 76.19 90

25 47 M S 2.1 41 4.21 4.23 100 3.61 3.74 104 84.47 88.42 108

26 34 M S 1.2 84 4.49 3.09 69 3.85 2.88 75 82.53 93.2 113

27 36 M N 1.3 62 4.49 3.09 69 3.85 2.88 78 82.53 93.2 113

28 42 M N 1.9 61 43 3 70 3.78 2.97 79 83.75 99 119

29 44 F N 1.7 75 4.64 6.07 131 4.02 5.55 138 83.61 91.43 109

30 47 F N 1.6 102 4.36 3.25 75 3.81 2.77 73 83.61 85.223 102

31 48 M N 1.7 112 4.32 3.25 81 3.86 2.86 82 82.35 88 107

32 33 F S 2.2 121 4.36 3.25 75 3.81 2.77 73 83.61 85.23 102

33 51 F N 1.9 124 4.64 6.07 131 4.02 5.55 138 83.61 91.43 109

34 57 F N 1.7 128 2.95 2.82 96 2.55 2.5 98 83.21 88.65 107

35 54 M N 1.7 111 4.36 3.28 78 3.81 2.77 73 83.61 85.23 102

36 51 M N 1.8 113 2.95 2.82 96 2.55 2.5 98 83.21 88.65 107

37 37 M S 1.6 98 3.69 2.31 63 3.22 1.76 55 84.73 76.19 90

38 32 M N 1.8 75 4.64 6.07 131 4.02 5.55 138 83.61 91.43 109

39 42 M N 1.7 86 2.95 2.82 96 2.55 2.5 98 83.21 88.65 107

40 51 M N 1.7 83 4.35 3.25 81 3.86 2.86 82 82.35 88 107

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KEY TO MASTER CHART

VEP - Visual Evoked Potential

RT - Right

LT - Left

BAEP - Brainstem Auditory Evoked

Wave Latency - I, II, III, IV, V

Inter Peak Latency - I-III, III-V, I-V

PFT - Pulmonary Function Test

CRP - ‘C’ Reactive protein

FEV1 -

Forced expiratory volume in one

second

FVC - Forced Vital Capacity