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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 6  |  Issue : 3  |  Page : 105-108

An investigative study on the impact of smoking on visual evoked response of healthy volunteers


1 Department of Physiology, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha, Maharashtra, India
2 Internship, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha, Maharashtra, India
3 Department of Anatomy, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha, Maharashtra, India

Date of Web Publication23-Oct-2018

Correspondence Address:
Ruchi Kothari
Department of Physiology, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha - 442 102, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcor.jcor_123_17

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  Abstract 


Background: Cigarette smoking not only has numerous deleterious effects on respiratory and cardiovascular systems of the body but also poses a threat to damage the visual system and may lead to poor eyesight. Visual evoked potentials (VEPs) reflect electrical phenomena occurring during the visual processing so are widely used both in research and in clinical practice to elucidate the function of the visual system. Aim of Study: To explore the effect of smoking on the VEP response of healthy volunteers. Materials and Methods: VEP recordings were taken using an Evoked Potential Recorder (RMS EMG. EP MARK II) where the stimulus configuration consisted of transient pattern-reversal method, in which a black-and-white checkerboard was generated (full field) on a VEP monitor. Results: The mean age of thirty smokers was 46.70 ± 17.33 years compared to 47.25 ± 15.62 years in 60 controls (range 19–76 years). Predominant P100 latency delays in 60% of cases, of which 55.56% had markedly prolonged latencies. Both latency delay and amplitude reduction were seen in remaining 40% of cases, i.e., 12 of 30 smokers. Marked prolongation of latency with marked amplitude reduction was observed in 9 (75%) of these 12 cases and all belonging to the most chronic smokers. Conclusion: To the best of our knowledge, ours is one of the first studies to comment on implications of smoking on VEP. As VEP abnormalities obtained in cases of smokers having extreme chronicity were severe, substantial, and explicit, we propose that VEP could be a useful neurophysiologic tool to demonstrate the visual deficits due to smoking.

Keywords: Smokers, tobacco, vision, visual evoked potential


How to cite this article:
Kothari R, Panchal V, Bokariya P. An investigative study on the impact of smoking on visual evoked response of healthy volunteers. J Clin Ophthalmol Res 2018;6:105-8

How to cite this URL:
Kothari R, Panchal V, Bokariya P. An investigative study on the impact of smoking on visual evoked response of healthy volunteers. J Clin Ophthalmol Res [serial online] 2018 [cited 2018 Dec 14];6:105-8. Available from: http://www.jcor.in/text.asp?2018/6/3/105/243840



Tobacco smoke is enormously harmful to one's health. Cigarette smoking is one of the major causes of cerebrovascular and cardiovascular complications in both developed and developing countries. It has been recognized as the third biggest risk factor for Indians.[1]

A Global Burden of Disease study,[2] coordinated by the Institute for Health Metrics and Evaluation based primarily on in-country surveys, government statistics, and the World Health Organization data, showed that there have been 1 million deaths in India due to tobacco smoking in the past decade.

A study published in the Journal of the American Medical Association examined the prevalence of smoking and cigarette consumption in 187 countries between 1980 and 2012 and found that in India, the percentage of men and women smoking is considerably high and over the past three decades 36.5 million new smokers have been added to the list (74.5 million in 1980 to 110 million in 2012).[3] According to the Global Adult Tobacco Survey,[4] 26% of adults in India consume smokeless tobacco in the form of khaini, kharrah, gutkha, jarda, etc. On an average, an Indian consumes 9 cigarettes/day and this figure does not vary much regionally.

It is by far well established that the smoking affects the blood flow. The major complications caused due to smoking are attributed to endothelial dysfunction, increased platelet function, inflammatory processes, hypercoagulability, and eventually atherosclerosis, leading to either structural or functional damage to the blood vessels. Many researchers quote that as smoking alters the normal circulation, it has significant effects on cerebral perfusion as well and may lead to alteration in physiology regulated by the area of brain suffering hypoperfusion.[5]

Smoking increases the risk of macular degeneration, cataracts, and poor eyesight. Of the 40,000 active substances in tobacco smoke, most are hazardous to human health. These toxic chemicals affect ocular tissues through ischemic or oxidative mechanisms.[6] Many common ophthalmological disorders such as retinal vein occlusion, age-related macular degeneration, cataract, anterior ischemic optic neuropathy, thyroid ophthalmopathy, and primary open angle glaucoma have been found to be associated with smoking. Diminished retinal sensitivity and peripheral scotomas in the visual fields have been observed in healthy heavy smokers.[7],[8]

The effect of smoking on visual pathway can objectively be very well observed through visual evoked potential (VEP). This is a quick neurophysiologic, low-cost, noninvasive test which assesses the functional integrity of visual system. Through this, the study tried to observe and analyze the alterations in VEP in smokers.

Aim

The aim of this study was to explore the effect of smoking on the VEP response of healthy volunteers. To accomplish it, VEP responses were recorded in a cohort of smokers and age-matched controls in the same age range and the results of smokers were compared with the with nonsmokers.


  Materials and Methods Top


This study was a case–control study conducted in the neurophysiology unit of the department of physiology of a rural medical college and associated with a tertiary care rural hospital located in a village of Central India. The study population consisted of participants in the age range of 18–76 years. A total of 30 cases and 60 controls were recruited. The sample size of 90 (60 controls and 30 cases) was determined by considering that 10% of unexposed population has abnormal VEP. It is known that 50% of alcoholics have abnormal VEP, helping us to make an expert estimation that 40% of smokers may have abnormal VEP, as most of the alcohol consumers are also smokers. Using all these figures in Epi Info7 (Centers for Disease control and prevention (CDC), Atlanta, Georgia, USA), the sample size came out to be 81. Considering 10% nonresponsive cases, we finally calculated a sample size of 90 for the present study.

All controls enrolled in the study were age and sex matched to the cases. Both cases and controls were healthy volunteers and were selected after proper screening as per the inclusion and exclusion criteria. Participants consuming not <15 cigarettes/day, aged 18 years or above, and having a history of smoking for at least 3 years were included as cases. Participants having no history of smoking, i.e., they were nonsmokers who did not smoke or they were abstinent from smoking, and who were aged 18 years or above were taken as controls. Patients having preexisting ophthalmic complication or retinopathies, lens/corneal opacities, miotic pupil, and recent eye medications (mydriatics or cycloplegics in the past 12 h), having a history of other neurological disorder or heart disease, hypertension, diabetes mellitus, and hyperthyroidism, who are not willing to participate, and any uncooperative or febrile patients were excluded from the study.

Baseline characteristics of all the patients were obtained. Demographic data, cardiovascular history, risk factors (hypercholesterolemia, hypertension, and diabetes mellitus), and prior significant events were recorded. We ruled out any other complications to state tobacco smoking as the only existing effector in the patients. We collected data with a structured questionnaire from all participants. We took complete clinical history and performed a physical examination and relevant investigation of pulse, temperature, blood pressure (BP), jugular venous pressure, pallor, icterus, skin turgor, tongue, pedal edema, peripheral pulsations, respiratory system, and cardiovascular clinical examination in all the study participants.

VEP recordings were done in accordance with the standardized methodology of the International Federation of Clinical Neurophysiology committee recommendations[9] and the International Society for Clinical Electrophysiology of Vision guidelines,[10] and montages were kept as per the 10-20 International System of electroencephalogram (EEG) electrode placements.[11] The reference electrode (Fz) was placed 12 cm above the nasion, the ground electrode (Cz) at the vertex, and the active electrode (Oz) at approximately 2 cm above the inion.

The stimulus configuration for VEP recording was transient pattern-reversal method, in which a black-and-white checkerboard was generated (full field) on a VEP monitor by an Evoked Potential Recorder (RMS EMG EP MARK II). The rate of pattern reversal (1.7 Hz), the size of the checks (8 × 8), the luminance (59 cd/m2), and contrast level (80%) were kept constant for all the recordings in all the cases and controls. The recording was done monocularly for the left and right eyes (LE and RE) separately with the participant wearing corrective glasses, if any during the test. Each participant was briefed previously about the procedure to alleviate any apprehension and to assure full relaxation during the test. Standard disc EEG electrodes were placed on the scalp areas after preparing the skin by degreasing and abrading with a conducting jelly or electrode paste (RMS recording paste) rubbed lightly into the area with a cotton swab to ensure good, stable electrical connection. The participant was seated comfortably at a distance of 1 m away from the screen of the VEP monitor so that the accommodation of eyes is relaxed.

The recording was done in air-conditioned, sound attenuated, darkened room. The only source of light was the stimulus itself. After controlling all factors that influence the VEP pattern, the participant was instructed to close one eye with black blinder on the eye and to fixate his other eye on a small red dot at the center of the screen of the VEP monitor, on which black-and-white checkerboard pattern is generated full field. The signals recorded were filtered (low-cut and high-cut-frequency filter) through a band spread of 2–100 Hz. The sweep duration was maintained at 300 ms. Responses to 200 stimuli were amplified and averaged for each eye, which were then analyzed by an Inline computer having automatic artifact rejection mechanism. A minimum of two records for each eye were obtained and superimposed on one another to ensure replicability of the VEP pattern.

The study parameters included P100 latency which is the time interval between the onset of a visual stimulus and the first maximum positive deflection or excursion of the VEP signal and P100 amplitude which is measured from the peak of N70 to trough of P100 wave.

All the data were directly fed into the computer and stored. Statistical analyses were performed using Statistical Package for the Social Sciences (SPSS) version 13.0 program (IBM Corp., New York, USA). Chi-square and independent t-tests were used to compare variables. Data were expressed as mean ± standard deviation (SD). P < 0.05 was considered statistically significant.

The study was approved by the institutional ethics committee when the protocol had been submitted for approval. The study began after getting the ethical clearance. Written informed consent was obtained from the patients before their enrolment in this study.


  Results Top


A total of 30 smokers and 60 controls were investigated for VEP. The mean ± SD values of the general characteristics including age, height, weight, pulse per min, and blood pressure of the cases and controls are summarized in [Table 1].
Table 1: Baseline characteristics of the study participants

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The mean age of smokers was 46.70 ± 17.33 years spanning in the range of 19–76 years. Control participants comprised 60 volunteers with age in the same age range (mean age 47.25 ± 15.62 years). The difference in the mean age as well as mean height of cases and controls was not statistically significant. The smokers have been compared to control group with regard to P100 latency and P100 amplitude of VEP on the right and left sides in [Table 2].
Table 2: Comparison between smokers and controls with regard to P100 wave latency and P100 amplitude in the right and left eyes

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Qualitative analysis of VEP waveform in smokers demonstrated predominant P100 latency delay in 18 of 30 smokers, of which 10 cases had markedly prolonged latencies. Both latency delay and amplitude reduction were seen in remaining 12 of 30 smokers. Marked prolongation of latency with marked amplitude reduction was observed in 9 of these 12 cases and all belonging to the most chronic smokers.


  Discussion Top


An increase in VEP latency clinically means degeneration in the quality of sight. VEP values have been evaluated in various ocular manifestations. However, to our knowledge, there is no study evaluating the effects of smoking on VEPs in the Indian subcontinent, especially in a rural set up like ours where the propensity of population with addiction of smoking is quite at a higher end. Hence, in this study, we aimed to evaluate the changes in VEP in participants with smoking addiction, so that it may help in the management of ophthalmological complications that may arise due to the ill effects of smoking. Once documented, we can raise awareness in the community regarding the deleterious effects of smoking on vision, especially in the youth. Damage related to cigarette smoking may begin soon after tobacco use initiation, reinforcing the preventive message that no level of smoking is safe in youth.

Keeping this in mind, in the present study, VEP was used as the neurophysiologic tool, measured in terms of P100 latency and amplitude in the study groups.

To evaluate the effects of smoking on VEP values, we compared the VEP results of smokers with nonsmokers. When VEP measurements were evaluated, it was seen that P100 latency values of both RE and LE were significantly higher in smokers than the control group. This finding is in concordance with another study by Sezer et al.[12] (2007) where they also reported prolongation of latencies in smokers; however, the values of P100 latencies were lower (108.3 ± 8.4 ms in RE and 107.8 ± 7.7 ms in LE) than those obtained in our participants (114.56 ± 6.72 in RE and 114.72 ± 6.74 in LE).

This prolongation of latency could be attributed to the impairment of neurovascular coupling caused by cigarette smoking which is primarily due to structural changes of the vessels as postulated by Boms et al.[5] (2010). This term defines a complex neurovascular control mechanism, during which neuronal activity evokes regional vasodilation and thus localized changes in blood flow in the brain.[13]

Further, it was revealed from the results that there occurred severe diminution of P100 amplitude in both eyes of the smokers when compared with controls. However, this observation differs from the study of Sezer et al. as they found no differences for any of the parameters measured between the groups except P100 latency.

Due to a paucity of literature in this particular area of research dealing with the effect of smoking and VEP, we did not have many reference studies to compare with. As per our results in younger cases, damage related to cigarette smoking may begin soon after tobacco use initiation, reinforcing the preventive message that no level of smoking is safe in youth.

The strength of the study lies in being the first in the Indian subcontinent to explore the variations of VEPs in smokers and also to have assessed noninvasive neurophysiological variables which reflect neural activity of visual system more directly than overt clinical indices. Yet, some of the limitations of the study are its small sample size and not being able to have a longitudinal assay of the chronic smokers due to time constraints.


  Conclusion Top


Smoking does produce obvious changes in pattern-reversal VEPs. Although it is a preliminary study, it surely is a pioneering attempt that provides evidence of alterations in VEP activity which have been statistically analyzed across participants under study. The increment of latency and attenuation of amplitude clearly manifests the visual function damage in smokers.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Boms N, Yonai Y, Molnar S, Rosengarten B, Bornstein NM, Csiba L, et al. Effect of smoking cessation on visually evoked cerebral blood flow response in healthy volunteers. J Vasc Res 2010;47:214-20.  Back to cited text no. 5
    
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Talhout R, Schulz T, Florek E, van Benthem J, Wester P, Opperhuizen A, et al. Hazardous compounds in tobacco smoke. Int J Environ Res Public Health 2011;8:613-28.  Back to cited text no. 6
    
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Friedman J, Meares R. Tobacco smoking and cortical evoked potentials: An opposite effect on auditory and visual systems. Clin Exp Pharmacol Physiol 1980;7:609-15.  Back to cited text no. 7
    
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Gundogan FC, Erdurman C, Durukan AH, Sobaci G, Bayraktar MZ. Acute effects of cigarette smoking on multifocal electroretinogram. Clin Exp Ophthalmol 2007;35:32-7.  Back to cited text no. 8
    
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Odom JV, Bach M, Brigell M, Holder GE, McCulloch DL, Tormene AP, et al. ISCEV standard for clinical visual evoked potentials (2009 update). Doc Ophthalmol 2010;120:111-9.  Back to cited text no. 9
    
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Celesia GG, Bodis-Wollner I, Chatrian GE, Harding GF, Sokol S, Spekreijse H, et al. Recommended standards for electroretinograms and visual evoked potentials. Report of an IFCN committee. Electroencephalogr Clin Neurophysiol 1993;87:421-36.  Back to cited text no. 10
    
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American Clinical Neurophysiology Society. Guideline 5: Guidelines for standard electrode position nomenclature. J Clin Neurophysiol 2006;23:107-10.  Back to cited text no. 11
    
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Sezer M, Yaman M, Oruç S, Fidan F, Ünlü M. Visual evoked potential changes in chronic obstructive pulmonary disease. Eur J Gen Med 2007;4:115-8.  Back to cited text no. 12
    
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Metea MR, Newman EA. Glial cells dilate and constrict blood vessels: A mechanism of neurovascular coupling. J Neurosci 2006;26:2862-70.  Back to cited text no. 13
    



 
 
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