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Doctoral dissertation
To be presented by permission of the Faculty of Medicine of the University of Kuopio
for public examination in Auditorium ML2, Medistudia building, University of Kuopio,
on Friday 25th January 2008, at 12 noon
Department of Physical Medicine and Rehabil itationKuopio University Hospital
Department of OtolaryngologyUniversity of Tampere
Department of Physical Medicine and Rehabil itationNorth Karelia Central Hospital , Joensuu
PÄIVI SUTINEN
Pathophysiological Effects of Vibrationwith Inner Ear as a Model Organ
JOKAKUOPIO 2008
KUOPION YLIOPISTON JULKAISUJA D. LÄÄKETIEDE 424KUOPIO UNIVERSITY PUBLICATIONS D. MEDICAL SCIENCES 424
Distributor : Kuopio University Library P.O. Box 1627 FI-70211 KUOPIO FINLAND Tel. +358 17 163 430 Fax +358 17 163 410 www.uku.fi/kirjasto/julkaisutoiminta/julkmyyn.html
Series Editors: Professor Esko Alhava, M.D., Ph.D. Institute of Clinical Medicine, Department of Surgery Professor Raimo Sulkava, M.D., Ph.D. School of Public Health and Clinical Nutrition Professor Markku Tammi, M.D., Ph.D. Institute of Biomedicine, Department of Anatomy
Author´s address: North Karelia Central Hospital Department of Physical Medicine and Rehabil itation Tikkamäentie 16 FI-80210 JOENSUU FINLAND Tel. +358 13 171 2890 Fax +358 13 171 2880
Supervisors: Professor Ilmari Pyykkö, M.D., Ph.D. Department of Otolaryngology Tampere University Hospital
Docent Olavi Airaksinen, M.D., Ph.D. Department of Physical Medicine and Rehabil itation Kuopio University Hospital
Researcher Jing Zou, M.D., Ph.D. Department of Otolaryngology Tampere University Hospital
Reviewers: Docent Marja Mikkelsson, M.D., Ph.D. Päijät-Häme Intermunicipal Federation for Social Services and Health Care Lahti
Docent Erna Kentala, M.D., Ph.D. Department of Otolaryngology Helsinki University Hospital
Opponent: Docent Karl-August Lindgren ORTON Invalidisäätiö Hospital Helsinki
ISBN 978-951-27-0944-1ISBN 978-951-27-1041-6 (PDF)ISSN 1235-0303
KopijyväKuopio 2008Finland
Sutinen, Päivi. Pathophysiological effects of vibration with inner ear as a model organ. Kuopio University
Publications D. Medical Sciences 424. 2008. 94 p.
ISBN 978-951-27-0944-1
ISBN 978-951-27-1041-6 (PDF)
ISSN 1235-0303
ABSTRACT Hand-arm vibration syndrome (HAVS) is a symptom entity that consists of disturbances in the
circulation of the fingers (Vibration White Finger or VWF), peripheral nerves of the hands and
arms, and possibly muscle, joint and autonomic nervous system disorders.
Changes in HAVS were assessed in a cross-sectional and in a longitudinal study of forestry
workers. Sensorineural and musculoskeletal symptoms were studied. Changes in vibrotactile
perception threshold were evaluated and the tonic vibration reflex was measured in
posturography. An animal model was created to assess inner ear damage after vibration
exposure.
The prevalence of vibration-induced white finger (VWF) decreased from 17 to 8 percent in
the cohort of 52 forestry workers. Numbness increased. Rotator cuff syndrome was diagnosed in
19% of men on the right side. Hand-arm vibration associated with the right rotator cuff
syndrome. Numbness was associated with pain in upper extremities.
Subjects with tension neck had excessive deviation of position in the lateral and
anteroposterior direction in posturography during and after vibration-induced stimulation of
neck and lumbar area.
In vibrotactile perception threshold measurement, tactile acuity worsened in the cohort study.
The threshold metric was the summed normalized threshold shift constructed for each subject.
The positive predictive value of the metric was 71%.
In an animal model, temporal bone vibration was used to assess the hearing loss caused by
vibration. After bone vibration 60 % of the guinea pigs developed a threshold shift exceeding 10
decibel (dB) at least at two frequencies. Exposure to vibration at higher frequencies (500-1000
Hertz, Hz) produced stronger TS than exposure to frequencies 32-250 Hz.
Temporal bone vibration caused expression of tumor necrosis factor alpha (TNF-α) and its‟
receptors (TNF R1, TNF R2) in the cochlea. The expression of TNF R2 was stronger than that
of TNF R1. Vibration also induced vascular endothelial growth factor VEGF and its‟ receptor
(VEGF R2) expression in the cochlea.
The results indicate that VWF and numbness have possibly different pathophysiological
mechanism. In the forestry workers, the strenuous work was associated with musculoskeletal
disorders and partly explains the numbness.
The animal model provides a new understanding of mechanisms leading to vibration-induced
cochlear changes and cellular damage. The frequency of vibration influences the threshold shift
of hearing in the vibrated cochlea. In the animal model, the expression of TNF-α and VEGF in
the vibrated cochlea seems to cause tissue remodeling. The inner ear changes may also model
vibration-induced damages in the hand-arm vibration syndrome. Shift to lower frequencies of
vibration is advisable. National Library of Medicine Classification: WA 400, WE 805, WV 270
Medical Subjects Headings: Biomechanics; Cochlea; Cohort Studies; Cross-Sectional Studies; Forestry;
Guinea Pigs; Hand-Arm Vibration Syndrome/etiology; Hand-Arm Vibration Syndrome/physiopathology;
Hearing Loss, Sensorineural; Mechanoreceptors/physiology; Musculoskeletal Diseases; Neck Muscles:
Innervation, Neck Pain/physiopathology; Occupational diseases; Occupational Exposure;
Posture/physiology; Receptors, Tumor Necrosis Factor type I, Receptors, Tumor Necrosis Factor type II,
Stress; Mechanical; Tumor Necrosis Factor- alpha; Vascular Endothelial Factor- alpha; Vascular
Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-1, Vascular Endothelial
Growth factor Receptor-2; Vibration/adverse effects
To Erkki, Laura, Tuuli, Martti and Anton
ACKNOWLEDGEMENTS
This study was carried out in conjunction with the Institute of Occupational Health,
Helsinki, Department of Otolaryngology of Karolinska Institute, Stockholm,
Department of Otolaryngology, Tampere University, Tampere, and Department of
Physical Medicine and Rehabilitation, North Karelia Central Hospital, Joensuu and
Department of Physical Medicine and Rehabilitation, Kuopio University Hospital.
I want to thank Medical Directors of North Karelia Central Hospital Pertti Palomäki
and Antti Turunen and former Head of Department of Physical Medicine and
Rehabilitation Eero Oura for kind support for my research. This work was financially
supported by the Forestry Workers Fund, Finnish National Board of Forestry, and the
Government special funds allocated to the North Karelia Central Hospital and Kuopio
University Hospital.
I am grateful for the forestry workers in Suomussalmi, who participated in this study,
and I appreciate the co-operation of occupational health services and Martti Seppänen in
Ämmänsaari. I express my sincere thanks to late colleague, my friend, Kaija Koskimies,
Ph.D., who asked me to join the research team in Suomussalmi study. She eagerly
helped me in the first steps of scientific studies and showed the way to go.
I am deeply indebted to my supervisor Professor Ilmari Pyykkö, Head of the
Department of Otolaryngology in Tampere University Hospital. He introduced the
world of scientific research to me. He constantly supported me throughout the years.
His inspiring personality and constructive criticism have carried me forward. Without
him this thesis would never have been finished.
I express my gratitude to my supervisor, Docent Olavi Airaksinen, Head of the
Department of Physical Medicine and Rehabilitation in Kuopio, for his valuable and
constructive comments on my work. I am also very grateful to my third supervisor,
researcher Jing Zou Ph.D., Department of Otolaryngology, Tampere University, for his
co-operation, enthusiasm and support. He created the first animal model to study the
vibration-induced hearing loss (2001), and he made the laboratory studies of the
immunohistochemistry in the animal model. He taught me to understand the nature of
hearing loss in the animal studies.
Special thanks to Esko Toppila, Ph.D., Institute of Occupational Health, Helsinki, who
gave me valuable advice in Physics. His kind friendship and help have been important
to me. He, together with Professor Jukka Starck, Head of Physics Department, Institute
of Occupational Health, has made the technical measurements of balance and animal
studies possible, for which I am very grateful.
I wish to thank Heikki Aalto, Ph.D., who made the recordings of postural stability and
who often encouraged me. I am also very thankful for Professor Anthony Brammer,
who made the recordings of the vibrotactile perception thresholds, and discussed the
topic of sensorineural changes thoroughly. I greatly appreciate his expertise and
friendliness. I thank Professor Lisa Hunter for her contribution in the hearing loss study.
I acknowledge the collaboration of Ulysses Diva, Ph.D. and Doctors Timo Hirvonen,
Risto Kaksonen, Hisayoshi Ischizaki and Professor Hannu Alaranta.
I sincerely appreciate the work of the reviewers Docent Marja Mikkelsson, Päijät-
Häme Intermunicipal Federation for Social Services and Health Care, and Docent Erna
Kentala, Department of Otolaryngology, Helsinki University Hospital, for their valuable
comments on my thesis.
I thank Doctor Jukka Alm for teaching the basics of statistics and statistician Pirjo
Halonen, University of Kuopio, and Professor Juha Alho, University of Joensuu, for
analyzing the study results with me. I express my gratitude to librarian Pirkko Pussinen
in North Karelia Central Hospital.
I am indebted to my colleague, Katri Laimi, M.D., Ph.D., for her continuous support
as a researcher and as a friend. I give my warmest thanks to my twin-sister Paula
Rajaniemi for helping me with secretarial work, my daughter Tuuli Gröhn for checking
the references and my friends Ilkka Jormanainen, Adele Botha, Antony Harfield, Ph.D.,
and Clint Rogers, Ph.D., for technical support. I am thankful to Marilyn Thompson,
M.Tchg., for her editing. I am indebted to colleagues and other staff in my Department
of Physical Medicine and Rehabilitation for allowing me to leave the daily work
because of the thesis. I express my deep gratitude to Liisa Mustala, M.D., for her
comments on the thesis and for hosting me in Tampere. During all these years, my
parents, sisters and children have supported and inspired me, for which I am truly
thankful. Finally I owe my deepest gratitude to my husband Erkki, for his enduring
encouragement, sense of humor and love. And I thank all of my friends for prayers,
because without miracles this thesis would not have been possible.
ABBREVIATIONS
ABR Auditory Brainstem Response
CGRP Calcitonin-gene related peptide
CSF Cerebrospinal fluid
CTS Carpal tunnel syndrome
dB Decibel
ENMG Electroneuromyography
FA-I Fast-adapting receptor I
FA-II Fast-adapting receptor II
FSBP% Percentage of finger systolic blood pressure
HAVS Hand-Arm Vibration Syndrome
Hz Hertz
IHC Inner hair cell
ISO International Organization for Standardization
OHC Outer hair cell
PBS Phosphate buffer saline
SA-I Slowly adapting receptor I
SA-II Slowly adapting receptor II
SD Standard deviation
SNHL Sensorineural hearing loss
SPL Sound pressure level
SSRE Shear stress response element
TN Tension neck
TNF-α Tumor Necrosis Factor alpha
TNF R1 Tumor Necrosis Factor alpha receptor 1
TNF R2 Tumor Necrosis Factor alpha receptor 2
TS Threshold shift
VAS Visual analogue scale
VEGF Vascular Endothelial Growth Factor
VEGF R1 Vascular Endothelial Growth Factor receptor 1
VEGF R2 Vascular Endothelial Growth Factor receptor 2
VPT Vibrotactile perception threshold
VWF Vibration-induced White Finger
LIST OF ORIGINAL PUBLICATIONS
I. Sutinen P, Toppila E, Starck J, Brammer A, Zou J, Pyykkö I. Hand-arm
vibration syndrome with use of anti-vibration chain saws: 19-year follow-up
study of forestry workers. Int Arch Occup Environ Health 2006; 79(8): 665-71.
II. Brammer AJ, Sutinen P, Diva UA, Pyykkö I, Toppila E, Starck J. Application of
metrics constructed from vibrotactile threshold to the assessment of tactile
sensory changes in the hands. Submitted for publication (Journal of the Acoustic
Society)
III. Koskimies K, Sutinen P, Aalto H, Starck J, Toppila E, Hirvonen T, Kaksonen R,
Ishizaki H, Alaranta H, Pyykkö I. Postural stability, neck proprioception and
tension neck. Acta Oto-Laryngol Suppl 1997;529:95-7
IV. Sutinen P, Zou J, Hunter LL, Toppila E, Pyykkö I. Vibration-induced hearing-
loss: mechanical and physiological aspects. Otol Neurotol 2007; 28(2): 171-7.
V. Zou J, Pyykkö I, Sutinen P, Toppila E. Vibration induced hearing loss in guinea
pig cochlea: expression of TNF-alpha and VEGF. Hear Res 2005; 202(1-2):13-
20.
The Roman numbers in the text refer to the above publications
TABLE OF CONTENTS 1 INTRODUCTION ..................................................................................................................... 15
2 LITERATURE REVIEW ......................................................................................................... 17
2.1 ENERGY PRINCIPLE OF VIBRATION DAMAGE ............................................................................. 17 2.2 ACUTE BIOLOGICAL RESPONSE TO VIBRATION EXPOSURE ........................................................ 18 2.3 HAND-ARM VIBRATION SYNDROME .......................................................................................... 18
2.3.1 Vascular changes: vibration-induced white finger ........................................................ 18 2.3.2 Sensorineural changes of HAVS .................................................................................... 22 2.3.3 Musculoskeletal changes ............................................................................................... 25
2.4 PREVALENCE OF HAND-ARM VIBRATION SYNDROME ............................................................... 27 2.5 PREVENTION OF VIBRATION DISORDERS ................................................................................... 28 2.6 PHYSIOLOGICAL RESPONSES OF VIBRATION AND NOISE............................................................ 29
2.6.1 Inner ear: cochlea .......................................................................................................... 29 2.6.2 Vestibulospinal system and postural stability ................................................................ 30 2.6.3 Vision and proprioception in postural stability ............................................................. 30 2.6.4 Cochlear injury: mechanisms of noise-induced hearing loss ........................................ 31 2.6.5 Animal model for vibration-induced functional changes ............................................... 33
3 PURPOSE OF THE STUDY .................................................................................................... 35
4 MATERIALS AND METHODS .............................................................................................. 36
4.1 SUBJECTS AND EXPERIMENTAL ANIMALS ................................................................................. 36 4.2 MEDICAL HISTORY ................................................................................................................... 36 4.3 MEDICAL EXAMINATION .......................................................................................................... 37 4.4 TESTS USED FOR ASSESSING MUSCULOSKELETAL FUNCTION IN 1995 ....................................... 38 4.5 MEASUREMENT OF VIBROTACTILE PERCEPTION THRESHOLDS .................................................. 38
4.5.1 Apparatus ....................................................................................................................... 38 4.5.2 Method ........................................................................................................................... 39 4.5.3 Metric for threshold shift ............................................................................................... 39
4.6 FORCE PLATFORM POSTUROGRAPHY ........................................................................................ 41 4.7 CALCULATION OF LIFETIME DOSE ............................................................................................ 41 4.8 ANIMAL EXPERIMENTS ............................................................................................................. 42
4.8.1 Vibration delivery .......................................................................................................... 42 4.8.2 Measurement of hearing ................................................................................................ 43 4.8.3 Analysis of cytokines with immunohistochemistry ......................................................... 44
4.9 STATISTICS ............................................................................................................................... 45
5 RESULTS ................................................................................................................................... 46
5.1 HAND-ARM VIBRATION SYNDROME WITH USE OF ANTI-VIBRATION CHAIN SAWS: 19-YEAR
FOLLOW-UP STUDY OF FORESTRY WORKERS (I) ...................................................................................... 46 5.1.1 Cross-sectional study ..................................................................................................... 46 5.1.2 19-year-cohort ............................................................................................................... 46
5.2 APPLICATION OF METRICS CONSTRUCTED FROM VIBROTACTILE THRESHOLD TO THE
ASSESSMENT OF TACTILE SENSORY CHANGES IN THE HANDS (II) ............................................................ 51 5.2.1 Summed normalized threshold shifts.............................................................................. 51 5.2.2 Summed normalized threshold changes ......................................................................... 53 5.2.3 The correlations between the threshold metrics, age and grip force ............................. 54 5.2.4 Prediction of numbness from summed normalized threshold shift................................. 55
5.3 POSTURAL STABILITY, NECK PROPRIOCEPTION AND TENSION NECK. (III) ................................. 55 5.4 VIBRATION-INDUCED HEARING LOSS: MECHANICAL AND PHYSIOLOGICAL ASPECTS (IV)......... 56
5.4.1 Transfer factor ............................................................................................................... 56 5.4.2 Threshold shift immediately following vibration ........................................................... 57 5.4.3 Recovery after vibration ................................................................................................ 58
5.5 VIBRATION INDUCED HEARING LOSS IN GUINEA PIG COCHLEA: EXPRESSION OF TNF-ALPHA
AND VEGF (V) ....................................................................................................................................... 59 5.5.1 Expression pattern of TNF-α in the vibration stimulated cochlea ................................. 59 5.5.2 Expression pattern of TNF receptors in the vibration stimulated cochlea .................... 59 5.5.3 Expression pattern of VEGF in the vibration stimulated cochlea .................................. 60 5.5.4 Expression pattern of VEGF receptors in the vibration stimulated cochlea .................. 60 5.5.5 Hearing loss after vibration ........................................................................................... 61
6 DISCUSSION ............................................................................................................................. 62
6.1 METHODOLOGICAL ASPECTS .................................................................................................... 62 6.2 CLINICAL ASPECTS OF VIBRATION- INDUCED HEALTH HAZARDS .............................................. 63 6.3 CLINICAL ASPECTS OF SENSORY THRESHOLD CHANGES ........................................................... 66 6.4 POSTURAL STABILITY AND NECK PAIN ..................................................................................... 67 6.5 INNER EAR AS A MODEL ORGAN FOR SENSORINEURAL DAMAGE ............................................... 68 6.6 UPREGULATION OF THE CYTOKINES DURING VIBRATION EXPOSURE ........................................ 70
7 CONCLUSION .......................................................................................................................... 71
8 REFERENCES ........................................................................................................................... 72
15
1 INTRODUCTION
Local vibration to hands occurs when the hands grasp vibrating tools and vibration
enters the body through the hands. Occupationally important sources of hand-arm
vibration are mainly prevalent in industry, construction or agriculture (Loriga 1911,
Pelmear 2003). Vibration is principally contacted with palm and fingers, but vibration
may be transmitted from hand to whole upper extremity and even further (Békésy
1939).
Long-lasting or excessive vibration has been associated with various disorders in
epidemiological studies. In 1911 Loriga reported that miners using pneumatic drills
suffered from attacks of vascular disturbances of finger circulation, the so called white
fingers (Loriga 1911). Since then Hamilton reported vasomotor disturbances in stone
cutters (Hamilton 1918, Hamilton 1930) and later other researchers reported the same
kind of disturbances in other users of vibrating tools; such as in airplane industry
workers, grinders, forestry workers and rock drillers (Dart 1946, Agate and Druett 1947,
Kylin and Lindström 1968, Seppäläinen 1972, Pyykkö 1974, Taylor et al. 1984, Starck
et al. 1984)
Hand-arm vibration syndrome (HAVS) consists of disturbances in the circulation of
the fingers (vibration white finger, VWF) and in the peripheral nerves of the hands and
arms (Seppäläinen 1972, Pelmear 2003). It may include muscle, bone and joint
disorders (Färkkilä 1978, Iwata 1968, Laitinen et al. 1974, Pyykkö 1986). Autonomic
nervous system involvement is not yet delineated. The symptoms of HAVS may either
coexist or occur separately.
In Nordic countries the symptoms of HAVS became alarmingly high in the middle of
the 1960‟s in forestry work. The prevalence of HAVS peaked in the early 70‟s, when
the prevalence of HAVS was 40-47 % (Hellström and Andersen 1972, Pyykkö 1974) in
forestry workers and it dropped to 5% in the 1980‟s (Koskimies 1992). VWF was also
common in foundry chipping/ grinding workers (with prevalence of 21%) in Italy
(Bovenzi et al. 1987), in pedestal grinders with a prevalence of 74-100% (Starck et al.
1983, Hayward and Griffin 1986, Seppäläinen et al. 1986), in rock drillers with
prevalence of 36- 50% (Chatterjee et al. 1978, Pelmear et al. 1987, Bovenzi et al. 1988).
Recently, in a large survey of metal workers, the prevalence of HAVS was 8.4% (Sauni
et al. 2006).
Different frequencies, durations and intensities of vibration exposure can cause
variable VWF and sensorineural changes (Griffin 2004). VWF and sensorineural
changes occur and progress independently (Pelmear 2003). Different tools have
different times of onset of symptoms, e.g. chain sawing with older type of chain saws
elicited HAVS in a few years (Koskimies 1992) in comparison with a longer latency of
new chain saws.
There is a classification of HAVS concerning VWF and neurological disorders,
according the Stockholm workshop scale. The purpose of the Stockholm workshop
scale is to standardize the classification of symptom intensity in order to compare the
different tools and frequencies causing HAVS. Vibrotactile perception threshold
measurement is one of the methods to analyze sensorineural symptoms.
16
Pathophysiology is not yet fully delineated (Chetter et al. 1998, Herrick 2005).
Vibration may induce structural changes in nerves and muscles. Vibration increases
perineural edema of epineural and endoneural connective tissue (Lundborg et al. 1987).
In rat tails, excessive vibration resulted in detachment of myelin sheath, deranged
paranodal regions and reduced nerve conduction (Chang et al. 1994). In neuromuscular
effects of vibration, studied by Necking et al (1996a), there is an increase of the cross-
sectional area of type I and IIC muscle fibers in comparison with controls. The muscle
nuclei are more centrally positioned (Necking et al. 1996b)
Takeuchi (1986) and Strömberg et al (1997) found demyelination of nerves and
perineural and perivascular fibrosis in vibration-exposed workers. In another study,
fractionated nerve conduction velocity across the carpal tunnel showed bimodal
distribution: one group had a carpal tunnel- like syndrome and the other group had a
more distal dysfunction (Rosen et al.1993).
In addition to vascular and neurological symptoms, musculoskeletal disorders also
occur after vibration exposure. In one study, a combination of muscle force, repetition,
elevated upper extremity posture and vibration exposure was associated with increased
prevalence of the rotator cuff tendonitis (Viikari-Juntura 1998). Musculoskeletal
disorders connected to vibration exposure need more research.
Whole body vibration occurs when the human body is supported on a vibrating
surface, e.g. in vehicles. Whole body vibration does not cause any generally accepted
diseases - except low back pain- and it is not included in this book.
The purpose of this study was to evaluate HAVS in a cohort of forestry workers, to
study changes of the postural stability during the vibration perturbation and to
understand the mechanisms leading to vibration-induced hearing loss and cellular
damage in the animal model. The inner ear damage model was used to provide insight
into vibration-induced disorder in the HAVS.
17
2 LITERATURE REVIEW
2.1 Energy principle of vibration damage
The references were searched from Medline and Pubmed in the beginning; during the
years, many searches were made with different search strategies, including the years
1911-2007.
The magnitude of vibration is usually measured by its acceleration (root mean square
value) and frequency (Griffin 2004). According to the standard, the risk is proportional
to the total vibration energy, i.e. magnitude and duration of exposure. The international
standard ISO 5349 uses frequency weighted values over the range of about 5 to 1500 Hz
(ISO 5349-1, 2001). The value given is that by which the vibration magnitude at each
frequency is multiplied in order to weight it according to its influence on the body. It
provides a model that can be used to predict the prevalence of VWF. Tominaga (2005)
reported that current weighting should be changed by way of weighting less to low
frequency and more to high frequencies.
The EU-legislation defines in directive (Directive 2002/44/EC) that the action limit
value is 2.5 ms-2
for 8 hr exposure. If this value is not exceeded, no protective actions
are required. The limit value for hand-arm vibration of 8-hour exposure is 5 ms-2
, which
cannot be exceeded at work. In addition, the directive requires that the effect of
vibration impulsiveness is taken into account. The harmfulness of impulsiveness has
been shown (Starck 1984, Starck and Pyykkö 1986) but so far no limit value has been
established. Exposure measurements should recognize that exposures are not
continuous, and that there may be some recovery between exposures.
A handle incorporating force and acceleration transducers was developed to measure
the energy transfer (Johnson 1975). It was shown that absorbed power (energy per time)
was 21 Nms-1
for rock drilling, and 2.7 Nms-1
for chiseling. The energy absorption
depends on time, gripping force, vibration magnitude and the type of tool (Burström and
Lundström 1994).
According to Dong et al. (2005), the hand-arm system had the greatest resonance in
the frequency rate of 20 to 50 Hz when testing biodynamic response. An increase of
applied force increased the magnitude of biodynamic response and vibration
transmission (Dong et al. 2005). No gender differences were reported (Bylund and
Burström 2003).
The amount of vibration energy, which is conveyed to the upper extremity, increases
linearly with increasing hand grip force (Starck 1984, Starck et al. 1990, Burström and
Lundström 1994). Low frequency (less than 50 Hz) impact vibration is absorbed up to
the elbow (Kihlberg and Hagberg 1997) and high frequency vibration (400 Hz) is
absorbed in the hand (Sörenssen and Burström 1997). Lidström (1973) suggested that
energy transfer to the hand is a better indication of vibration-induced damage than the
measurement of acceleration. She showed the correlation between energy absorption
and HAVS (Lidström 1973).
18
2.2 Acute biological response to vibration exposure
Vibration causes physiological changes in sensibility, motor control and blood
circulation (Griffin 2004). Exposure to the static load does not cause any changes in
finger blood flow (Bovenzi et al. 1995b, 1997b). Vibration at 125 Hz leads to temporary
vibration- induced vasodilatation in the vibrated finger in healthy males, and later on, in
recovery period, to cold-induced vasoconstriction, i.e. reduced finger blood flow in the
ipsilateral and contralateral fingers. The mechanisms involve both local vasodilatation
and central sympathetic reflex vasoconstriction activity (Bovenzi et al. 1995b). Also a
reduction in toe blood flow is associated with vibration of the hand (Egan et al. 1996).
The extent of decrease in digital blood flow is dependent on frequency of vibration
(Bovenzi and Griffin 1997).
The longer the duration of vibration exposure and the higher the magnitude of
vibration, the longer was the vasoconstriction response (Bovenzi et al. 1998a, Bovenzi
et al. 1999, Bovenzi et al. 2000a).
After short-term exposure to vibration, temporary threshold shift (TS) for vibrotactile
perception threshold (Maeda and Griffin 1993, Maeda 1994, Maeda and Griffin 1995,
Malchaire et al. 1998a, Malchaire et al. 1998b), two-point discrimination (Bovenzi et al.
1997a) and nerve conduction impairment was reported (Nohara et al. 1986, Malchaire et
al. 1998b). After half an hour‟s vibration exposure, temporary TS‟s occur in vibration
perception threshold (VPT), and paresthesia and numbness develop; TS‟s increase
concomitantly with vibration acceleration (Malchaire et al. 1998a, Malchaire et al.
1998b). Also sensorimotor reflexes such as tonic vibration reflex have been reported to
be altered (Martin and Park 1997).
In a study of muscular function in arm and shoulder muscles during vibration
exposure, Rohmert et al (1989) found that the EMG (electromyography) index shows
increase of 39% in trapezius muscle and to a lesser extent in infrapinatus, biceps and
lower arm extensor muscles. The prime movers are most affected by vibration (Rohmert
et al. 1989).
2.3 Hand-arm vibration syndrome
2.3.1 Vascular changes: vibration-induced white finger
HAVS consists of:
1. vascular changes (VWF),
2. sensorineural changes,
3. possible bone and joint changes and
4. other possible changes, e.g. autonomic nervous system changes.
The first two, vascular and sensorineural, changes can be classified according to the
scales (see below).VWF consists of blanching of fingers starting from distal phalanges
at the onset of symptoms (Hamilton 1918, 1930, Agate and Druett 1947, Pelmear 2003).
19
When exposure to vibration continues, the blanching can extend to proximal phalanges
of fingers. Among forest workers it may occur for example after years of professional
chain sawing, and is provoked by cold or damp weather (Pyykkö 1974). The attacks
occur mostly in winter and may last from a few minutes to over one hour (Pyykkö 1974,
Pelmear 2003). Attacks are shortened by warming. The duration varies with the
condition of the environment and the intensity of the vasospasm, and the VWF attack
then ends when the whole body is warmed (Pyykkö 1986). When warming occurs,
blanching is followed by vasodilatation with hyperemia and pain (“hot aches”). In
extremely rare cases, blanching may lead to trophic changes as ulceration or gangrene
of the fingertips. During the attacks of VWF the workers can lose the touch sensation
and manipulative dexterity (Sakakibara et al. 2005, Cederlund et al. 1999). Proper
clothing and lunches in heated lodges reduced number and severity of VWF in Finnish
forestry workers‟ population (Koskimies 1994). Smoking may influence hand-arm
vibration syndrome (Cherniack et al. 2000).
A scale for grading VWF has been proposed by Taylor and Pelmear (1975, refer table
1), and it was revised in a workshop in Stockholm (Gemne et al. 1987) to separate
vascular and neurological scaling and to eliminate seasonal criteria. It also tried to
eliminate subjective scaling in the workplace and in the home.
Table 1. The Taylor-Pelmear scale for the classification of vibration-induced white
finger
Stage Condition of digits Work and social interference
0 No blanching No complaints
0T Intermittent tingling No interference with activities
0N Intermittent numbness No interference
1 Blanching of one or more fingertips,
with or without tingling or numbness No interference
2 Blanching of one or more fingers,
with numbness, usually in winter
Slight interference with home
and social activities
3 Extensive blanching: frequent episodes in
summer as well as in winter
Definite interference at work, home
and with social activities,
restriction of hobbies
4 Extensive blanching : frequent episodes in
summer and winter
Occupation changed to avoid
further vibration due to symptoms
20
Table 2. Stockholm workshop scale for the classification of vibration white finger
Stage Severity Condition of digits
1 Mild Occasional attacks affecting only the tips of one or more fingers
2 Moderate Occasional attacks affecting distal and middle phalanges of fingers
3 Severe Frequent attacks affecting all phalanges of most fingers
4 Very Severe As in stage 3, with trophic skin changes in finger tips
The Stockholm Workshop Scale was published in 1987 (Gemne et al. 1987, refer table
2). The Stockholm Scale has been criticized for encompassing the highly subjective
interpretation of frequent attacks and low sensitivity of early asymptomatic vascular
injuries (Ishitake et al. 1995, Noel 2000).
2.3.1.1 Laboratory investigations of vascular changes
Several laboratory tests have been used in assessment of VWF. Most of them are
based on cold provocation and measurement of skin temperature or digital blood flow.
Plethysmography can be used to evaluate the pulse wave forms in digital arteries pre-
and post-cold stress.
Cold provocation involves immersion of the hands in cold water (10-15 degrees). In
measurement of cold provocation, the blood pressure is measured from finger (Juul and
Nielsen 1981, Olsen et al. 1985). If the blood pressure is reduced more than 50% in
comparison to blood pressure measured in 30°C, the result is diagnostic (Sauni et al
2006). There is a correspondence of test results and clinically staged symptoms in over
70% of cases (Juul and Nielsen 1981, Gemne and Pyykkö 1986). Finger systolic blood
pressure measurement can also compare the affected finger pre-and post-cold blood
pressure with the thumb, which is usually not affected (Olsen and Nielsen 1979).
Finger systolic blood pressure is compared with the pressure of the arm (Ekenvall and
Lindblad 1986b) after cooling the hand. Decreased systolic blood pressure of the
affected finger indicates reduced circulation. Pyykkö et al. (1986a) compared the
method of measurement of finger systolic blood pressure to a test in which arms and
body are cooled and whitening of the digits is observed. The measurement of finger
systolic blood pressure seemed to be more acceptable to patients and easier to
standardize (Pyykkö et al. 1986a).
Laser Doppler perfusion imaging has been studied in response to a cold provocation
test. VWF patients had significantly lower values than controls during the last minutes
of cold provocation (10 degrees) and the following recovery time (Miyai et al. 2005).
Pyykkö et al. (1986b) used laser Doppler to identify vasomotor control abnormalities in
VWF patients. The diagnostic value of the laser Doppler system has not been
established.
Finger skin temperature measurement is a quick and less costly method and it
correlates with digital blood flow in various water temperatures, but measurement in air
is unreliable because it is dependent on environmental factors, e.g. the room
temperature. Despite this fact, finger skin temperature measurement has been used after
21
cooling the finger (Juul and Nielsen 1981, Bovenzi 1987, Yamada et al. 1995, Lawson
and Nevell 1997). Cherniack et al. (2003) reported that finger skin temperature recovery
after cold provocation in VWF subjects remained reduced even if the subject had
stopped vibration exposure years ago.
Infrared thermometry measurements of skin temperature rewarming time after cold
provocation has also been used (Vonbierbrauer et al. 1998, Coughlin et al. 2001). The
finger tip temperatures of HAVS patients remain significantly lower than pre-cooling
values during a 10 minute-rewarming period (Coughlin et al. 2001). This method is
relatively insensitive to provide discrimination between controls and HAVS patients.
2.3.1.2 Pathophysiological aspects of vascular changes
Pathophysiology of vascular changes in HAVS is not yet fully delineated (Chetter et
al. 1998, Herrick 2005). Takeuchi has reported arterial smooth muscle hypertrophy and
fibrosis between endothelium and internal elastic lamina of blood vessels (Takeuchi et
al. 1986, 1988).
Functional vascular abnormalities have been reported: an imbalance between a potent
vasoconstrictor, endothelin 1, and calcitonin-gene related peptide (CGRP), which is a
powerful vasodilatator (Palmer and Mason 1996, Goldsmith et al. 1994). In VWF there
is a loss of CGRP neural fibers leading to predominance of endothelin 1 (Goldsmith et
al. 1994). In VWF patients, a cold challenge is connected with an increase in endothelin
1-concentrations compared to healthy subjects (Palmer and Mason 1996).
There may also be impaired production of other vasodilatators such as NO (Nitric (II)
oxide) and prostacyclin (Teh et al. 1995, Palmer et Mason 1996, Rajagopalan et al.
2003). Increase in peripheral resistance has been reported (Futatsuka et al. 1983, Gemne
et al. 1986, Pyykkö and Gemne 1987) in the fingers of subjects with VWF during heat-
induced vasodilatation.
The circulation of fingers involves cholinergic, adrenergic and serotoninergic
receptors in vasoregulatory systems (Lindblad and Ekenvall 1990). Several researchers
have reported changes in the adrenergic function. Vasoconstriction to norepinephrine is
mediated through α1- and α2- adrenoreceptors (Ekenvall et al. 1988), and during cold-
induced vasoconstriction the normally silent α2C -adrenoreceptors redistribute from
Golgi compartments to the cell surface (Jeyaraj et al. 2001). It may occur that, in
patients with VWF, there is a lower set up-point for α2C-adrenoreceptors. Acute
vibration increases alpha2C-adrenergic smooth muscle constriction (Krajnak et al 2006).
Also, α1- adrenoreceptor damage may lead to α2- adrenoreceptor predominance and
strengthen vasoconstrictor response (Ekenvall and Lindblad 1986, Issley et al. 1995,
Stoyneva et al 2003).
The autonomic nervous system may contribute to vascular changes of occupational
origin (Harada 1994). Olsen et al. (1985, 1987) and Pyykkö (1986) proposed that the
central sympathetic drive closes the main digital arteries. Single hand vibration induces
contralateral vasoconstriction (Bovenzi et al. 1995a) and even vasoconstriction of feet
(Sakakibara et Yamada 1995, Egan et al. 1996). Intravascular abnormalities have also
been reported (Herrick 2005). Both central and peripheral mechanisms seem to exist.
Vasoconstriction is aggravated by cold weather (Govindaraju et al. 2006); a warm
climate leads to smaller prevalence of VWF (Yamamoto et al. 2002).
22
2.3.2 Sensorineural changes of HAVS
Numbness of the hands and arms or a tingling in fingers and deterioration of finger
tactile perception has been found in workers exposed to vibration (Seppäläinen1972,
Araki et al. 1976, Brammer and Pyykkö 1987, Dahlin and Lundborg 2001). Numbness
is generally reported during and after exposure. Numbness is common especially during
night time (Färkkilä et al. 1985, Burke et al. 2005).
Prevalence of peripheral neurological changes varies from a few percent to more than
80 percent of vibration-exposed workers (ISO5349-1). In population sample of 12,907
vibration-exposed workers, 2,607 (20.2%) reported sensory symptoms, numbness or
tingling. Sensory symptoms were associated with hand-arm vibration (Palmer et al.
2000). In a group of dental hygienists using high frequency ultrasound hand pieces,
44.7% of them had paresthesia (Cherniack et al. 2006). The sensorineural changes are
more common than vascular changes (Letz 1992, Virokannas 1995, Strömberg et al.
1996) and they have shorter latencies than vascular symptoms (Behrens et al. 1982).
Sensorineural symptoms are usually reversible. However, they may also be irreversible
(Bovenzi et al. 1994). Vibration may lead to a reduction of normal perception of touch
and temperature, and manual dexterity (Sakakibara et al. 2005). Clinical tests as
pinprick, light touch, 2- point discrimination and tuning fork testing are relatively
insensitive and associated with developed lesions (Dellon 1980, Szabo et al. 1984).
Cederlund et al. (1999) reported that the majority of HAVS patients found activities of
daily living difficult, especially handling manual tools, handwriting, lifting objects,
buttoning clothes and handling book. The Purdue Pegboard Test measures dexterity and
gross movements of hands, fingers and arms. The Purdue pegboard test showed reduced
hand function in 17 out of 20 workers (Cederlund et al. 1999). Low performance in a
bean transfer test (picking up beans) was associated with increasing vibrotactile
perception threshold and decreasing grip strength in Sakakibara et al‟s (2005) study;
buttoning clothes and picking up small objects were difficult in HAVS patients. This
might be attributed to impaired sensory feedback from SAI (Slowly adapting receptor I)
and FAI (Fast adapting receptor I) afferents in glabrous skin. A classification system for
severity of sensory changes has been proposed (Gemne and Saraste 1987), according to
Stockholm Workshop Scale. Pelmear and Kusiak (1994) and Pelmear (2003) proposed
that stage 4 should be included in the Stockholm sensorineural classification for patients
with abnormal Tinel‟s and nerve conduction tests.
Table 3. Stockholm workshop scale of sensorineural stages
Stage Symptoms
0 SN Exposed to vibration but no symptoms
1 SN Intermittent numbness with or without tingling
2 SN Intermittent or persistent numbness, reduced sensory perception
3 SN Intermittent or persistent numbness, reduced tactile discrimination and/or
manipulative dexterity
Table 3 key: SN= sensorineural stage
23
In a study from a heavy engineering company, with the average tool use being 23.3
years, the individual cold provocation test did not associate with the Stockholm
workshop scale, but neurological tests did associate with sensorineural staging.
Vascular changes associated with age and total hours of vibration (McGeoch and
Gilmour 2000). Also, perception of touch and dexterity showed a moderate association
with sensorineural staging, as well as cold intolerance and pain in the upper limbs
(Cederlund et al. 2003).
2.3.2.1 Laboratory investigation of sensorineural changes
Neurological function can be tested with ENMG (Chatterjee et al. 1982, Brammer and
Pyykkö 1987, Rosen et al. 1993, Sakakibara et al. 1998, Strömberg et al. 1999) and
VPT‟s (Werner et al. 1995, Strömberg et al. 1998, Lundström et al. 1999, Strömberg et
al. 1999). Thermal perception threshold testing seems to be useful in examining small
nerve fiber injuries in HAVS. Warm thresholds tend to elevate and cold thresholds tend
to lower (Toibana et al. 2002).
The vibrotactile and thermal threshold impairments require specific testing
(Strömberg et al. 1999): severe small fiber injuries of neurons can occur in the absence
of nerve conduction abnormalities (Flodmark and Lundborg 1997, Ekenvall et al. 1989,
Cherniack et al. 1990).
Electroneuromyography (ENMG)
Fractionated nerve conduction studies are important in assessing compressing
neuropathies and large fiber neuropathies (Strömberg et al. 1999). Seppäläinen (1972)
reported neuropathy in HAVS patients. Distal latency was lengthened and conduction
velocities shorter in motor neurons (Seppäläinen 1972). Both sensory and motor
conduction velocities were reduced in other studies (Juntunen et al. 1983, Brammer and
Pyykkö 1987). Digital sensory nerve conduction is slowed in more than 40% of patients
with VWF (Sakakibara et al. 1998).
Carpal tunnel syndrome (CTS) may coexist with vibration-related neuropathy. In 47
vibration-exposed men the distal latency of median nerve was moderately increased, but
it was less than in CTS patients. One group showed significant reduction in carpal
tunnel and the other group more distal dysfunction (Rosen et al. 1993). It has been
confirmed by others (Sakakibara et al. 1998).
CTS was found in 26% of forestry workers by ENMG in 1988 (Färkkilä et al. 1988).
This has been confirmed by others (Miller et al. 1994, Pelmear and Taylor 1994). Burke
et al. (2005) reported that 15 per cent of 26 846 HAVS patients, miners, had also CTS.
Recently it has been reported, that HAVS subjects having CTS had a great impact on
their perceived ability to do everyday tasks and on their reduced quality of life, both
physical and mental components (Poole and Mason 2005).
Vibration-related neuropathy in the arms seems to constitute a separate entity:
multiple- site- segments of the median and ulnar nerves, mainly distally to the wrist, are
impaired (Sakakibara et al. 1998, Giannini et al. 1999, Bovenzi et al. 2000b, Cherniack
et al. 2004). Reduced sensory nerve conduction velocity of radial nerve was reported in
Japan in HAVS patients (Hirata et al. 2002)
24
Vibrotactile perception threshold (VPT)
The sense of touch in the glabrous skin of the hands is mediated by neural activity in
up to four populations of mechanoreceptors, which may be differentiated
physiologically on the basis of their morphology, and functionally on the basis of their
responses to static and dynamic skin indentation (Vallbo and Johansson 1984, Johnson
2001, Brammer et al. 2007).
Table 4. Mechanoreceptors
Anatomical
population Function
Frequency
(Hertz)
FAI Meissner corpuscles Gripping and holding
objects 20-35
FAII Pacinian corpuscles Sensitive to vibration 100-400
SAI Merkel discs Detection of surface
features 0.5-6
SAII Ruffini endings Respond to skin stretch -
Table 4 key:
FAI = Fast-adapting receptor I
FAII=Fast-adapting receptor II
SAI =Slowly adapting receptor I
SAII=Slowly adapting receptor II
Aatola et al. used an accelerometer to measure VPT from the middle finger of the left
hand (Aatola et al. 1990). The vibration of a small plastic tip was pushing the fingertip
by a constant force, and the vibration increased continuously. When feeling the
vibration, the person pressed a switch in his right hand. When doing this, the switch
immediately returned the vibration to null, and the vibration began again increasing.
The vibration was measured from frequencies of 63, 125 and 250 Hz. The vibration was
measured three times for each frequency, and the mean of these values was seen as a
VPT. The temperature of the fingertip was also checked. Lundström (1985) showed that
VPTs were elevated on the hands of therapists, who used ultrasound vibrators operating
at 1 MHz, which is an exceptionally high vibration frequency.
Vibration sensitivity of fingertips, as measured with VPT, is reduced in patients with
HAVS (Coutu-Wakulczyk et al. 1997, Strömberg et al. 1998, Lindsell et al. 1999,
Sakakibara et al. 2005, Brammer et al. 2007). Cederlund et al. (1999) reported that in
the Semmes-Weinstein monofilament test, the small object shape identification and
moving 2-point discrimination tests were indicating an abnormal outcome in activities
of daily living, such as handling tools or books, handwriting and buttoning clothes. The
tested males had worked with vibrating tools for a mean duration of 24 years
25
(Cederlund et al. 1999). The best predictors of the change in tactile acuity were
difficulty in manipulating small objects and buttoning clothing (Coutu-Wakulczyk et al.
1997).
Normative data of VPT and thermal thresholds have been published (Lindsell and
Griffin 2002). A number of other sensorineural tests have also been applied (Kent et al
1998). Thermal thresholds as well as pain thresholds can be used to detect small nerve
fiber injury testing in vibration-induced neuropathy (Ekenvall et al. 1986a, Toibana et
al. 2000, Nilsson and Lundström 2001, Sakakibara et al 2002) Nevertheless,
quantitative sensory testing lacks standardization in the population of hand-arm
vibration neuropathy: it is susceptible to the effects of test methodologies (Lundström
2002). Age, outdoor or indoor temperature are confounding factors (Lindsell and Griffin
2002).
Vibrotactile and thermal impairments should be measured, because ENMG does not
show even severe small fiber injuries in HAVS (Ekenvall et al. 1989, Flodmark and
Lundborg 1997, McGeoch et al. 2004) Thermal and vibrotactile perception
measurements are correlated in vibration-exposed workers (Lindsell and Griffin 1999,
Strömberg et al. 1999, Toibana et al 2000). Vibrotactile perception measurements are
not in daily use yet, but mainly used in scientific studies. Quantitative sensory testing is
used by neurologists, e.g. in North America.
2.3.2.2 Pathophysiological aspects of peripheral nerve changes
Pathophysiological mechanism in sensorineural symptoms is not evident (Dahlin and
Lundborg 2001). Biopsies have been taken from nerves (Hashimoto and Craig 1980,
Takeuchi et al. 1986, 1988, Lundborg et al. 1987, 1990, Strömberg et al. 1997).
Vibration increases perineural edema of epineural and endoneural connective tissue
(Lundborg et al. 1987).
Chang et al. (1994) found detachment of myelin sheath, constriction of the axon, and
accumulation of vacuoles in peripheral nerves of rat tails exposed to vibration. These
findings were confirmed by Ho and Yu (1989) and Lopata et al. (1994). Ultrastructural
changes as deranged axoplasmic structure of plantar nerves could be seen to normalize
in 4 weeks after vibration in the hind leg of rats (Lundborg et al. 1990).
The vibration-damaged local nerve endings lead to neuronal loss, especially in the
perivascular nerves in fingers containing CGRP (Goldsmith et al. 1994, Bunker et al.
1996), which is a potent vasodilatator.
Takeuchi et al. (1986) found demyelination of nerves and perineural and perivascular
fibrosis greater in vibration-exposed workers than in controls. Because of vibration
exposure, structural nerve changes were reported in humans at wrist level: breakdown
of myelin and interstitial and perineural fibrosis (Strömberg et al. 1997). Diffuse
neuronal loss with neuropathy can extend from fingers to wrist, explaining poor
recovery after carpal tunnel release (Strömberg et al. 1997).
2.3.3 Musculoskeletal changes
Muscle-related disorders been reported after vibration exposure by subjects (Griffin
2004). Bovenzi et al. (1991) reported dose-effect relationship of vibration exposure with
26
the bicipital tendonitis and epicondylitis in forestry workers. In another epidemiological
study, a combination of muscle force, repetition, elevated upper extremity posture and
vibration exposure was associated with an increased prevalence of the rotator cuff
tendonitis (Viikari-Juntura 1998). There is difficulty in establishing the rotator cuff
syndrome associated with vibration only. There are many confounding factors for neck
and upper extremity musculoskeletal disorders as awkward postures, ageing, heavy
manual work and traumas (Hagberg 2002).
Åström et al compared the prevalence of HAVS and musculoskeletal symptoms in
769 professional drivers of snow mobiles, and reindeer herders with randomly selected
296 male referents. Increased odds of musculoskeletal symptoms were reported in the
areas of wrists, shoulders and neck with cumulative vibration exposure (Åström et al.
2006).
Workers using low-frequency impact tools (less than 50Hz) in comparison with
workers using non-impact tools (e.g. forest workers) reported more elbow and shoulder
disorders (Bovenzi 1987, Kihlberg and Hagberg 1997). The workers with high-
frequency impact tools (over 50 Hz) reported more wrist symptoms, which may be
caused by the fact that high frequency impact vibration is attenuated in the hand and
wrist (Kihlberg and Hagberg 1997).
Bone and joint changes have been reported (Laitinen et al. 1974, Stenlund et al. 1992,
Bovenzi et al. 1987) but conclusive evidence is still lacking (Gemne and Saraste 1987).
Use of percussive pneumatic tools, with the repetitive frequency around 30 Hz, may be
connected with bone and joint disorders (Lie 1980, Bovenzi 1987). For example, stone
quarry workers with chipping hammer use were reported to have radiographic changes
in the right elbow (Sakakibara et al. 1993).
Forestry workers with VWF may lose more grip force in comparison to other forestry
workers (Matsumoto et al. 1977, Färkkilä 1986, Sakakibara et al. 2005). Muscular
fatigue assessed by maximal voluntary contraction has been found to be dependent on
age and exposure to vibration and to be partly secondary to vibration-induced
neuropathy (Inaba et al. 1993). Necking et al. (2002) reported that vibration-exposed
workers presented weaker extrinsic and intrinsic muscle forces than the controls.
2.3.3.1 Pathophysiological aspects of muscle changes
In the hind paws of rats exposed to vibration of 80 Hz, different degrees of
degeneration were reported in plantar muscles as well as signs of regeneration. No
changes were reported in contralateral limbs (Necking et al. 1992). In vibrated rat hind
limbs, a strong increase of Insulin-like Growth Factor-1 was found in the anterior
tibialis muscle and a less striking increase in the Achilles tendon (Hansson et al. 1988).
It was concluded that vibration can induce reactive changes in tendon fibroblasts, which
are located locally in the vibrated limb (Hansson et al. 1988).
Pathological changes in hand muscles in man have been reported (Necking et al.
2004). The main morphological changes included centrally located myonuclei, fiber
type grouping, angulated muscle fibers, fibrosis and regenerating fibers. The changes
were associated with cumulative vibration exposure (Necking et al. 2004).
27
2.4 Prevalence of hand-arm vibration syndrome
In Sweden, 11% of working men reported using hand-held vibrating tools at least half
of their working day (Ekenvall et al. 1991).
The main causes of hand vibration are the tools used in metal industry, forestry,
construction and mining. The use of these equipments may lead to HAVS variably
(Table 5).
There are also differences between occupations, work places and individuals e.g. in
working material, grip forces, body position, and susceptibility to attain HAVS when
using vibrating tools (Bovenzi 1998b, Färkkilä et al 1985, Gemne and Lundström
1996).
Table 5. Tools potentially leading to HAVS and their vibration level (latency in
years) in 1968-1986. The name of the author, tool, year of publication, number of
study population, and prevalence of vibration induced white fingers (VWF) are
shown. In latency evaluation above the symbol ‘–‘ indicates data not available.
Study Tool Year Number VWF
(per cent)
Latency
(years)
Iwata Mining 1968 225 72 -
Partanen Pneumatic drills 1970 41 70 -
Chatterjee et al. Pneumatic rock drills 1978 42 50 1-19
Taylor et al. Quarry hammer 1984 30 80 -
Brubaker et al. Rock drill 1986 58 45 1-14
Among 344 shipyard workers, 22.7% of them had vascular symptoms and 78.2% of
them had sensorineural symptoms according to the Stockholm workshop scale in Korea
(Jang et al. 2002). Hill found that 50% of miners had HAVS in Canada (Hill et al.
2001). On the contrary, in Hungary 78.9% of 95 foundry workers had vascular and
65.3% had sensorineural symptoms (Kakosy et al. 2003). VWF was reported in 24% of
car mechanics and 25% of them had numbness (Barregard et al. 2003).
28
Table 6. Prevalence and mean latency of vibration-induced white finger in chain
saw users in 1972-1992
Study Year Number VWF
(per cent)
Latency
(years)
Hellström et al. 1972 296 47 1-18
Pyykkö 1974 118 40 4
Pyykkö et al. 1981 203 27 -
Härkönen et al. 1984 279 18 -
Färkkilä et al. 1988 186 5-22 -
Koskimies et al. 1992 124 5 2.5-6.6
There is a trend of reduction in the prevalence and severity of VWF in forestry
workers as demonstrated in table 6. HAVS has decreased because of several factors as
change in vibration level (see chapter 4.7), environmental factors (as meals in warm
environment, proper clothing, and transportation) and hygienic measures.
2.5 Prevention of vibration disorders
In Finland about 6% of workers were exposed to hand-arm vibration in 2002.
Vibration can be reduced by the use of preventive managerial, technical and individual
measures (Griffin 2004). Use of vibration reduced working procedures can be planned
ahead, e.g. instead of vibrating impact wrenches, drillscrewers are recommended. Tools
should be designed not to require tight grip or strong push forces. Vibration reduced
machinery can be designed, e.g. the use of an auto-balancing system in grinders
(Cockburn 2006). Vibration reduction can be achieved by using anti-vibration grips, e.g.
in chain saws (Koskimies et al. 1992) and pneumatic chisels. Grip coatings can be made
of rubber or of other elastic material. Technical staff should be able to assess the amount
of vibration, and equipment should be used and maintained properly (Griffin 2004).
It may be beneficial to allow breaks between vibration exposures, and all workers
exposed to hand-arm vibration should be warned about adverse effects of HAVS. In the
risk assessment of HAVS, the effect of impulsive vibration and individual susceptibility
must be taken into account. All the staff should be screened before and during the
exposure of vibration at regular intervals to ensure early identification. Occupational
health care should be alert in identifying HAVS. The worker himself can wear adequate
clothing to avoid symptoms in a cold environment. Workers with vibration exposure
should avoid smoking.
In Finland enactment of the work safety, on the ground of the EU-legislation directive
(Directive 2002/44/EC), regulates the measurement of vibration, the preservation of
29
exposure level assessment and risk analysis, prevention of vibration exposure and
guiding of the exposed workers.
2.6 Physiological responses of vibration and noise
2.6.1 Inner ear: cochlea
Sound is a fluctuation of air pressure which induces pressure waves and the sensation
of hearing (Bekesy 1932). Loudness is related to the sound pressure of the vibration.
Amplitude is measured on a logarithmic scale in decibels (dB). The middle ear, i.e. the
tympanic membrane and ossicular chain, convert vibrations from the air to pressure
changes inside the inner ear fluids (Luxon 2003, Evans 2003). The stapes footplate in
the oval window transforms the air pressure changes to fluid oscillation into the
vestibular scala. The change is transmitted across the cochlear partition to the round
window in the scala tympani. The pressure changes in cochlea produce traveling waves
in the basilar membrane. The basilar membrane in its‟ basal portion has minimum width
and maximum stiffness. For high frequencies of noise, the traveling wave is limited to
Hand-Arm Vibration Syndrome
Exposure of vibration: duration and intensity, impulsiveness
Environmental factors
Hand-grip force
Ergonomic factors
Susceptibility and genetic factors
Preventive measures
Figure 1. Factors involved in Hand-Arm Vibration
Syndrome
30
the basal portion. The apex has maximum width and lowest stiffness. For low
frequencies of noise, the traveling wave is maximal in apex (Evans 2003).
Both the inner hair cells (IHC) and the outer hair cells (OHC) respond to the fluid
oscillation but have different sensitivity. (Fridberger et al 2002). The outer hair cells in
the organ of Corti act like electro-mechano transducers (Brownell 2006). As a result, the
movement of the OHC changes the rigidity of basilar membrane and related structures.
The compliance of vibrating Organ of Corti in the area corresponding to the specific
frequency is increased. The organ of Corti is tuned to enhance the sensitivity of the
inner hair cells to the specific sound sequence. This tuning is further improved at a
different exchange station in the brain stem and finally in the cortex. As the end result,
the fine tuned signal generated by the inner hair cells is conveyed to the brain from the
cochlear nerve fibres to perceive the sound (Evans 2003).
2.6.2 Vestibulospinal system and postural stability
The vestibular system consists of otoliths and semicircular canals. Vestibular hair cells
are also mechanoreceptors, that is, they sense head position change. The otoliths seem
to operate at low frequency range, usually below 0.2 Hz. They detect linear acceleration
such as gravity. The semicircular canals are capable of detecting angular acceleration of
head, at frequencies of 0.5-6 Hz (Nashner 1971). The contribution of vestibular
information is to maintain visual image by controlling the eyes and to stabilize the head
in space (Wilson and Peterson 1978). Vestibulospinal reflexes control skeletal muscular
responses for the maintenance of adequate posture. The unilateral loss of vestibular
function causes a strong but usually transient postural asymmetry.
Visual, vestibular and proprioceptive systems contribute to postural control and
interact with one another. Afferent proprioceptive information and vestibular input
converge in brainstem. It has been shown that one of the key areas in animal studies is
the central cervical nucleus in the brainstem (Ragnarsson 1998). The role of central
cervical nucleus in man is not delineated yet (Massazza 1923).
2.6.3 Vision and proprioception in postural stability
Vision is important but not essential in postural control (Brandt et al. 1986). Postural
sway is greater when eyes are closed than when eyes are open and this difference is
used in postural stability assessment by determining the Romberg's quotient (Hytönen et
al. 1993). Visual stabilization depends on eye-target distance (Paulus et al. 1984).
To maintain postural balance during stance, postural corrections must be made
continuously. Spindle afferent provide proprioceptive information that is used to trigger
spinal reflexes automatically in fast corrections to transient, postural disturbance.
Continuous upright stance regulation needs sensory feedback at low frequencies 0.3-1.0
Hz.
Proprioception is used to detect changes in position or movement of one part relative
to another part of the body. Proprioceptive receptors are situated in muscles, tendons
and joints (Enbom 1990). Muscle spindles are located in the muscle, and arranged
parallel to the fiber. Each muscle fiber may have several muscle spindles. The number
31
of muscle spindles is dependent on the task of the muscle. The stretching of the muscle
and active muscle contraction activates the primary endings, which are branches of
primary group Ia afferent nerve. The activation of primary endings releases a stretch
reflex, which is monosynaptic. The reflex facilitates activity of the agonistic muscles
and inhibits the activity of antagonistic muscles. Muscle stretching also activates the
secondary endings. They are disynaptically connected to spinal α-motoneurons and also
give information about the muscle tension to higher motor control centers of the central
nervous system (Eklund and Hagbarth 1966, Prochazka and Hullinger 1983).
Golgi tendon organs are proprioceptors between muscle tendon fibers. They are
activated both by active muscle contraction and by passive tendon stretch. Activation of
Golgi tendon organs reverses the response of muscle spindles: it facilitates the
antagonistic muscles and inhibits the action of agonistic muscles. This may be a defense
mechanism protecting the muscles from excessive loading and a fine tuning mechanism
(Enbom 1990). Joint receptors are situated in or near the joint capsule. Activation
occurs by joint movement and by the stretching of muscles attached to the joint capsule.
Most afferents seem to be activated only in extreme angular displacements (Enbom
1990). Exteroceptive receptors, as presso- and mechanoreceptors, are situated in the
subcutaneous tissue. They can be divided into slowly adapting (SA) or fast adapting
type (FA) receptors.
The pressor receptors can sense stretching of the skin (Johansson et al. 1980). The
receptors in the sole of the foot have capacity to sense pressure changes to detect the
change in postural sway (Johansson et al. 1982).
Several studies have shown that cervical proprioception has a significant effect on
orientation and posture (Pyykkö et al 1989, Revel et al.1994, Karlberg et al 1995). Neck
pain patients with or without cervical root compression showed poorer postural
performance in vibration-induced body sway (Karlberg et al. 1995). Revel et al. (1991,
1994) showed that tension neck patients with pain have reduced sensitivity of neck
proprioception. If the initial position of head was to be re-assumed after maximal
rotation to the side, the neck patients performed significantly poorer than healthy
controls (Revel et al. 1991).
2.6.4 Cochlear injury: mechanisms of noise-induced hearing loss
Noise is excessive auditory stimulation and it elicits shear forces in cochlea. Noise
may damage the Organ of Corti, Reissner‟s membrane, basilar membrane and lateral
wall of cochlear duct (Ulehlova 1983). There are two different ways that lead to
cochlear injury: mechanical and metabolic (Ulehlova 1983).
Intense noise (exceeding 120 dB SPL) in animals may also mechanically disrupt
cochlear structures. At a lower sound pressure level, the sound can result in disturbed
cochlear homeostasis and functional impairment (Scheibe 1992) by releasing free
radicals (Salvi et al. 2001). When the metabolic or mechanical stress is too strong,
apoptosis or necrosis occurs and cell death ensues (Ylikoski et al. 2001). Apoptosis can
be seen as a counterbalance to cell division. Apoptosis does not affect the surrounding
tissues.
32
Necrosis leads to disorganized breakdown of the cell, with a subsequent inflammatory
process in the surrounding tissue (Leon et al. 2004). Pye and Ulehlova (1989) noted that
intense noise caused drastic changes initially in the first row of OHC, followed by IHC
and then the change spreads to all rows in affected area. When mechanical or metabolic
stress is too high, permanent hearing loss is a result (Pyykkö et al. 2007).
Changes in blood flow have been considered to contribute to that sensorineural
hearing loss, SNHL (Nakashima et al. 2003). Lamm and Arnold have reported noise-
induced hearing-loss has been found parallel to a change in cochlear blood flow causing
local ischemia (Lamm and Arnold 1996). The reduced pressure of oxygen is connected
with accumulation of metabolites and functional alterations. The exact role of
diminished cochlear blood flow is unclear and cochlear hypoxia may precede it (Lamm
and Arnold 1996).
During intensive noise trauma, there is an excessive release of the transmitter
substance of hair cells, most likely the release of glutamate. It is toxic on nerve endings
and elicits an inflow of calcium ions and subsequent swelling of the nerves. This
mechanism may be involved in noise-induced hearing loss of the IHC (Puel et al 1998).
Figure 2. Mechanisms of necrosis and apoptosis
Modified from Pyykkö et al. (2007).
Prevention of damage to the inner ear function after noxious agents has been an area
of intensive research. SNHL is known to occur after acoustic traumas. Drilling of the
temporal bone during surgery exposes the cochlea to both noise and vibration
(Hamernik 1989). The incidence of SNHL following surgeries involving drilling of the
temporal bone has been reported to be between 3 to 5% in large series (English et al.
1973, Palva et al. 1973, 1976, Smyth et al. 1975). Others have reported even higher
rates of slight post-operative SNHL, up to 55% in standard audiometric frequencies
(Man and Winerman 1985, Domenech et al. 1989, Vasama 2003).
GLUTAMATE
NECROSIS
SHEAR STRESS
TEAR
METABOLIC STRESS
CELLULAR OXYGENATION BLOOD FLOW CHANGE
DAMAGE
CELL DEATH
APOPTOSIS
33
Variables such as drill speed, burr size and type, and site of drilling have been
systematically investigated on isolated temporal bones, cadavers and an animal model
(Paparella 1962, Kylen et al. 1977, Gjuric 1997). The characteristics of the drill
variables and time domain of skull vibration determine the amount of vibration
exposure.
Noise exposure up to 125 dB in drilling (Holmquist et al. 1979, Kylen and Arlinger
1976, Urquhart et al. 1992) alone seems insufficient to cause permanent SNHL in
patients, and other factors such as vibration and actual trauma to the ossicular chain may
be as, or more, important than noise (Pyykkö et al. 1986c, Pyykkö et al.2003).
2.6.5 Animal model for vibration-induced functional changes
2.6.5.1 Up-regulation of growth factors in noise trauma
Cells exposed to vibration or mechanically active environment respond with
morphological changes caused by tangential shear forces. This cell response is called
shear stress. For example endothelial cells alter their morphology, growth rate, and
metabolism in response to fluid shear stress (Stamatas and McIntire 2001).
There are two general ways in which the mechanical signals may be transmitted from
the cellular membrane to the nucleus to induce gene regulation. One way is through
cytoskeletal structures from the cellular membrane to the nucleus, intracellular
junctions, and focal adhesion points (Stamatas and McIntire 2001). The other way is
through diffusible secondary messengers released locally close to the membrane. These
include, for example, calcium ions, adenosine triphosphate (ATP), mitogen-activated
protein kinase (MAPK), and a variety of other protein kinases.
Resnick et al. (1993) first reported that endothelial cells exposed to uniform laminar
shear stress up-regulate a shear stress response element (SSRE). Nuclear factor-κB (NF-
κB) could functionally interact with the SSRE (Khachigian et al. 1995). According to
the consequent research, several additional SSREs were reported later. Among these is
early growth response-1 (Egr-1), which interacts with Platelet-Derived Growth Factor-
A, and activator protein-1 (AP-1), (Khachigian et al. 1997, Shyy et al. 1995). Recent
research has shown that vascular endothelial growth factor (VEGF) and the receptors
are also involved in fluid induced shear stress response (Gan et al. 2000, Milkiewicz et
al. 2001, Abumiya et al. 2001, Conklin et al. 2002).
In vitro study Abumiya evaluated shear stress of vascular endothelial cells and
demonstrated increased VEGF R2 expression (2001). The authors interpreted this as
showing that an increase in the shear stress in the vasculature by post-ischemic
reperfusion stimulates a VEGF R2 expression, resulting in an increase in vascular
permeability and leading to neo-vascularisation. The newly formed myofibroblasts
express VEGF and VEGF R2 that seem to play a significant role in tissue
repair/remodeling after myocardial infarction (Chintalgattu 2003)
VEGF expression in connection to shear stress seems to be dependent on time. After
longer shear stress, its expression is increased up to 14 days (Gan 2000, Milkiewicz et
al. 2001).
34
In the cochlea, the hair cells are activated by shear movement in the organ of Corti
during sound stimulation (Fridberger et al. 2002). In noise or vibration trauma, shear
stress related response might be active in the cochlea and so lead to abnormal signal
transduction. Tumor necrosis factor (TNF)-α is involved in cell damage mechanism
especially through TNF receptor 1 (p55), while TNF receptor 2 (p75) can induce
activation of c-Jun NH2-terminal kinases (JNK) and NF-κB (Goeddel 1999). The
activation of JNK and NF-κB has the function of an anti-apoptotic agent. (Heldin and
Purton 1998). When both receptors are expressed, the activation of TNF receptor 2
enhances the effects of receptor 1 activation. Also VEGF may be involved in the
survival of the inner ear cells by enhancing the transport over the inner ear barrier (Zou
et al. 2005, Fraenzer et al 2006).
VEGF may also mediate its neural protection by upregulating Glial cell line-derived
neurotrophic factor expression (Gao et al 2005). Glial cell line-derived neurotrophic
factor has been found 8 hours after noise exposure, and it is involved in stress response
in the cochlea (Nam et al. 2000). Glial cell line-derived neurotrophic factor is protective
of noise induced cellular damage (Keithley 1998, Ylikoski et al. 1998).
35
3 PURPOSE OF THE STUDY
In the present study, the purpose was to evaluate pathophysiological effects of
vibration, especially:
I. to evaluate the changes in the HAVS findings of forestry workers. Special
interest was focused on neck, upper arm and forearm musculoskeletal disorders
and their association to HAVS
II. to detect threshold changes in tactile acuity over the five-year period. Changes
were compared with measurements of hand grip, and with neurological
symptoms among forestry workers
III. to examine the changes of the postural stability during perturbation of neck and
lumbar proprioceptors with vibration exposure
IV. to determine the hazardousness of different frequencies of vibration: using the
inner ear as a model organ
V. to evaluate mechanisms leading to functional and structural vibration-induced
damages: using the inner ear as a model organ
36
4 MATERIALS AND METHODS
4.1 Subjects and experimental animals
I. A cross-sectional medical examination was carried out with 109 men in 1995. A
cohort of forestry workers (n=52) was elected who were examined in each of
examinations between 1976 and 1995 (subgroup 1).
II. 18 forestry workers were examined as a cohort in 1990 and 1995 (subgroup 2)
III. A cross-sectional examination was carried out in 1995 with 106 forestry
workers, in connection with a compulsory medical examination (subgroup 3; 3
out of 109 subjects did not participate in postural stability measurements )
IV. Thirty pigmented guinea pigs of both sexes, weighing 400 – 760 g with normal
Preyer‟s reflexes were used.
V. Twelve male and female guinea pigs, weighing from 250 g to 500 g, were used
in the study. Seven animals were exposed to transcranial vibration and five
animals were used for control. Six animals of the vibration group and four
animals of the control group were used for sectioning with
immunohistochemistry. One animal in the vibration group and one in the control
group were used for surface preparation with immunohistochemistry.
4.2 Medical history
(I-III) Total vibration exposure was recorded during each survey totaling 11 visits in
Suomussalmi County. The work of the forestry workers involved operation of
lightweight chain saws for up to ten months per year. The forest workers felled and de-
branched trees (typically 25 - 35 cm diameter at the base), and were paid by piecework.
All forestry workers were employed by the same employer. The study was combined
with a compulsory medical examination.
Detailed enquiries of medical history were taken with the aid of a structured
questionnaire designed at the beginning of the cohort and the questionnaire was used in
all study occasions. The questions were related to personal medical history and
smoking. Special attention was given to an occupational history of vibration exposure
and to the symptoms and signs of HAVS. The diagnosis of VWF was made according
to the typical history of well-demarcated blanching of fingers after exclusion of primary
Raynaud‟s phenomenon. Other possible causes of secondary Raynaud‟s phenomenon
were excluded. If the forestry worker had not had an attack of VWF for at least two
years, he was considered to have inactive VWF.
Peripheral sensorineural disturbances such as numbness with tingling or paresthesias
of hands and arms were explored as well as any subjective loss of handgrip force.
Numbness was classified as present if persistent and troublesome. Each subject
underwent a medical interview concerning neck and upper extremity pain. Pain in neck,
upper arm, forearm, and wrist-hand regions during preceding 12 months were enquired.
Intensity of cervical and lower back pain during the past 2 weeks prior to the
37
questionnaire was rated by a horizontal visual analogue scale (VAS) ranging from 0 to
100 mm (Huskisson 1982). Routine laboratory tests were made (erythrocyte
sedimentation rate, hemoglobin). The routine tests did not lead to further investigations.
In this follow-up study the basic questionnaire stayed the same. Prevalence of HAVS
was earlier evaluated with cold provocation test in this group. It also included random
sampling to exclude false negative results (Pyykkö et al 1986a).
4.3 Medical examination
(I-III) The clinical examination of musculoskeletal disorders was performed by two
physicians specialized in physical medicine and rehabilitation. Special attention was
given to musculoskeletal neck and upper extremity disorders. A neurological
examination of the upper extremities was conducted on all subjects, including
sensorimotor function of the upper extremities. Cervical motion was measured with a
Myrin goniometer. Clinical musculoskeletal diagnoses were modified from the criteria
provided by Waris et al. (1979). No subject had a fracture of the cervical spine or upper
extremity, or any malignant diseases of the neck-upper extremity.
Table 7. Criteria for clinical diagnoses of musculoskeletal disorders
Modified from Waris et al 1979
Tension neck
Feeling of fatigue or stiffness in the neck, neck pain or headache radiating
from the neck, at least two tender spots or palpable hardenings and muscle
pain or tightness upon neck movement
Rotator cuff
syndrome
In symptom cases, typical history of painful arch and intermittent pain and
pronounced tenderness locally in the shoulder region were diagnostic
or
In addition, at least one of the following signs: painful arch test during
elevation, pain in resisted abduction or resisted external rotation.
Epicondylitis
syndrome
In symptom cases, a typical history of activity-dependent pain in the
epicondyle region and local pronounced tenderness at the lateral or medial
epicondyle were diagnostic,
or
A local pain during rest and/or movement, local tenderness at the lateral or
medial epicondyle and local pain on resisted wrist extension (lateral) or
wrist flexion (medial).
Duration of the
symptoms
in this study
Symptoms (pain, ache, or numbness) were present at the time of the
medical examination or in the preceding last 30 days
38
4.4 Tests used for assessing musculoskeletal function in 1995
Handgrip forces were evaluated with a Jamar dynamometer (Jamar Ltd, Canada).
Upper extremity functional tests developed by Soukka et al. (1989) were performed.
In this assessment the validated scores ranged from 1-5 and reflected age-related
muscular performance of upper limbs. The static test consists of timing how long a
standing person can hold a single 10 kg load in both hands in arm‟s length and at
shoulder height (up to a maximum 90 sec). The dynamic test consists of counting how
many times a person can repeatedly elevate two 10 kg loads, one held in each hand,
from shoulder height to full arm extension above the head when standing erect. The
performance is evaluated separately in the dynamic test (Soukka et al. 1989). These
tests were performed by local occupational health care nurses.
4.5 Measurement of vibrotactile perception thresholds
Figure 3. Tactometer
4.5.1 Apparatus
Non-invasive measurements of mechanoreceptor-specific vibrotactile thresholds were
performed at the fingertips using a tactometer. The device has been described elsewhere
39
(Brammer et al. 2007), and consists of: 1) a vibration stimulator suspended from a beam
balance, the fulcrum of which is mounted on a vertically adjustable track; 2) an arm
rest; 3) a small diameter (3 mm) cylindrical probe through which the stimulus is applied
to the skin; 4) an accelerometer and electronics to record the stimulus at the surface of
the skin, and; 5) a computer to administer the stimulus consisting of pulsed sinusoidal
tone bursts, and calculate perception thresholds.
The tone bursts were 800 ms in duration at frequencies of 20 Hz, and above, and 1.6 s
in duration at frequencies of 6.3 Hz, and below. The quiescent interval was 0.6 s.
Successive bursts initially increase in intensity until stimulus has been detected (“upper”
threshold). Successive bursts then decrease in intensity until the stimulus can no longer
be felt, so defining the first descending or “lower” threshold. The threshold limit was
detected using the Bekesy technique, which was repeated four times. The mean
threshold acceleration was calculated from the arithmetic sum of ascending and
descending thresholds.
4.5.2 Method
The subject was seated with his forearm and hand supported horizontally below
shoulder level, and positioned on the armrest for maximum comfort. This was achieved
by adjusting the elbow angle and rotating the wrist. The stimulator was positioned so
that a 3 mm diameter, cylindrical, flat-ended probe could be lowered onto a fingertip
and maintained in contact with the skin with a static compressive force of 0.05 N.
Pulsed vibrotactile stimuli were then applied to the skin at amplitudes close to the
threshold of perception, according to the algorithm. The skin-stimulator contact
conditions and stimulation frequencies were chosen to elicit responses from the SAI (4
and 6.3 Hz) or FAI (20 and 32 Hz) mechanoreceptor populations (Brammer and Piercy
2000). The measurement procedure was first explained to the subject, together with the
sensations he was likely to feel. Several practice runs were performed to familiarize the
subject with the stimuli and measurement procedure. Thresholds were determined at the
fingertips of digits 3 and 5 of both hands.
After extending the metrics for individual fingers to hands, and to subjects (i.e.,
combining data for both hands), the threshold changes are compared with hand grip
force and age. The VPT measurements were made by one person (Professor Anthony
Brammer). The validity of the test was tested earlier (Brammer et al. 1992).
4.5.3 Metric for threshold shift
(II) When all thresholds are expressed in dB, the summed normalized threshold shift at
a fingertip, TSSum(SD) , can be written (Brammer et al. 2007):
Equation 1
)()()( SDFAISDSAISDSum TSTSTS
Here the metric has been expressed in terms of the mean normalized threshold shifts
recorded in each receptor population, TSSAI(SD) and TSFAI(SD), where SD stands for
standard deviation:
40
Equation 2
SAISAISDSAI SDTSTS )(
and TSFAI(SD) has been equivalently defined. The mean receptor-specific threshold
shifts from the values observed in healthy hands, TSSAI and TSFAI, are first calculated
for each finger from:
Equation 3
23.64 TSTSTSSAI and
Equation 4
23220 TSTSTSFAI
where the threshold shift at a given frequency, TS4, at 4 Hz, etc., is the difference, in
dB, between the observed threshold and the mean threshold recorded from the hands of
healthy persons at that frequency (Brammer et al. 1993).
When expressed in dB, the thresholds for a population of healthy persons may be
approximated by a Gaussian distribution for each frequency. As the range of thresholds
for frequencies mediated by the same receptor population are similar, or identical, the
distributions may conveniently be expressed in terms of the standard deviation (SD) of
their means, which are written SDSAI and SDFAI, for the SAI and FAI distributions,
respectively.
The threshold at a fingertip is then considered „normal‟ (N) if its value of TSSum(SD)
falls within 1.96 standard deviations of the mean value recorded in the hands of healthy
persons (i.e., p > 0.05). The sensitivity is considered „marginal‟ (A) if the value of
TSSum(SD) falls within the parts of the distribution defined by (two-sided) probability
values in the range 0.005 < p < 0.05, and „abnormal‟ (AA) if it falls within the parts of
the distribution defined by (two-sided) probability values in the range 0.0005 < p <
0.005. Values of TSSum(SD) that fall within the tails of the threshold distribution for
which p < 0.0005 are considered to be „very abnormal‟ (AAA).
The threshold changes during the five year interval between studies have been
estimated, for each finger, from the summed mean threshold change, TCSum, which
becomes, when all thresholds are expressed in dB (Brammer et al. 2007):
Equation 5
FAISAISum TCTCTC
In this expression, TCSAI and TCFAI are the mean threshold changes for thresholds
believed mediated by the SAI and FAI receptor populations, respectively, and are
constructed from the threshold changes observed at each measurement frequency using
expressions equivalent to equations 3 and 4 (e.g., with TC replacing TS, and TCSAI
replacing TSSAI , etc.). The threshold change for each finger at each frequency is the
difference between the thresholds recorded from the same finger in the two studies.
41
4.6 Force platform posturography
(III) The movement of the centre point of force was measured with a force platform
(Starck et al. 1993). Relative displacement of the body position while standing and
during vibration perturbation of muscles in the neck, lumbar region or calf was studied.
The test condition was randomized according to Latin square design.
In the neck stimulation, two vibrators were placed paravertebrally beside the seventh
vertebra and attached with elastic bands over the stimulated muscles. For lumbar
stimulation, two vibrators were positioned paravertebrally on the erector spinae muscle.
For stimulation of calf muscles, a vibrator was placed firmly with elastic bands on the
calf muscles. Following stimulation frequencies were used (their duration plus length of
subsequent stimulation-free period): 32 Hz (12 s + 15 s) and 50 Hz (12 s + 15 s). The
test was performed by a physicist. Validity of the test was tested earlier (Starck et
al.1993).
4.7 Calculation of lifetime dose
(I) On the basis of the estimated periods of time of chain saw use, a lifetime vibration
dose for each forestry worker was calculated, where aw is the frequency weighted
acceleration (ms –2
), th is the individual estimated daily exposure (hours/day), and td the
number of working days in a year and ty is the number of years of saw use.
The lifetime dose was calculated using the equation 6 (modified from Bovenzi,
1995c):
Equation 6
)())(( 4
22
12
8
2 hdttt
as
myd
hw
Vibration was measured on the front and rear handles of the chain saw used in the
forest districts. In order to assess the total exposure, data used from the previous surveys
in the area since 1976, were reanalyzed. For vibration measurements, the accelerometers
were fastened into the front and rear handles of the chain saw. The signals were
amplified with a charge amplifier (Bruel and Kjaer 2635, Denmark). From the one-third
octave band vibration spectra (6.3-1250 Hz), the root mean square (rms) of the
frequency-weighted acceleration was calculated.
A commonly used chain saw was used to model vibration for each generation of chain
saws. The first generation chainsaws, used before 1972, had daily usage time of 2.5
hours with vibration level 9.1ms-2
. The second-generation anti-vibration chain saws
were used until the early 1980‟s 3.5 hours/day and the vibration level measured from
the handle was 2.2 ms-2
. After the early 1980‟s, the third generation chainsaw with a
vibration level of 1.8-2.2 ms-2
were used for 4.5-5 hours/day according to measurement
(Koskimies 1992).
42
4.8 Animal experiments
Power amplifier
LD-vibrometer
Spectrum analyzer
Charge amplifier
Accelerometer
Vibrator
Vibrating probe
Temporal bone
Figure 4. Schematic drawing of vibration exposure
Thanks to Professor Ilmari Pyykkö for allowing to use this schematic drawing.
4.8.1 Vibration delivery
(IV, V) The animals were initially anaesthetized with xylazine (Rompun® 16mg/kg
i.m.) and ketamine (Ketalar® 60mg/kg i.m.). The anaesthetized guinea pig was placed
in a specially designed holder. A vibrating system consisting of an electromagnetic
shaker with a probe (Ling TPO 1, Ling Industries, England), signal generator and power
amplifier (Ling TPO 1, Ling Industries, England) was used. The frequency and intensity
of the vibration could be adjusted. The vibration was delivered to the external ear canal
of the guinea pig from the shaker through a custom made probe (Zou et al. 2001). To
obtain equal pressure between the vibration probe and the animal‟s head, we used a
balance beam with extra weight of 100g at the shaker‟s side (IV). The weight against
the skull was selected to be of the same order of magnitude as the head of the guinea pig
to ensure a maximum impedance match between the head and the rod. At the selected
frequency range this should have only a minor effect on transmission.
43
(IV) Vibration frequencies were 32 Hz (n=5), 63 Hz (n=5), 125Hz (n=5), 250Hz
(n=5), 500Hz (n=5), and 1000Hz (n=5), and vibration time was 15 min for each animal.
Shaft vibration levels of the shaker ranged from 11 to 215 ms-2
at different frequencies.
The skull velocities were measured and converted to acceleration (a) by the equation 7.
Thus the respective stimulus acceleration of temporal bone was 4.2-18.8 ms-2
. The
vibration measurements were calibrated using a standard calibration (Zou et al.2001).
Equation 7. Acceleration
a=2·π·f·v
Equation 7 Key:
a= acceleration, f= frequency, v=velocity
(V) Seven animals were subjected to 15 minutes of vibration at 250 Hz with a linear
acceleration of 6 ms-2
measured from the temporal bone with laser vibrometer (Bruel
and Kjaer 2815, Denmark).
4.8.2 Measurement of hearing
(IV) Auditory brain stem response (ABR) recordings were performed with an
electrophysiological recording system (SigGen system 2, Tucker-Davis Technologies,
Gainesville, USA) in an electrically shielded, soundproof chamber. The ABR was
recorded in the same ear that received the vibration exposure. A subdermal (active)
needle electrode was inserted at the vertex, and the reference electrode was placed at the
ipsilateral mastoid. The ground electrode was placed at the contralateral mastoid.
Preamplifier filters were set at 30 Hz (high pass) and 3000 Hz (low pass). Tone bursts
(1ms-1
rise/fall; 0.5, 1, 2, 4, 8, 16 kHz) were used to measure the animals‟ ABR
thresholds. Stimuli were fed to a TDH-39 transducer connected to a tube fitted to the
external ear canal. ABR thresholds were obtained at 20 dB steps and finally at 5 dB
steps to identify the lowest level at which an ABR response could be visually
recognized (Pratt 2003). The hearing threshold was measured before vibration,
immediately after vibration, 7 days after vibration, and 14 days after vibration.
(V) The bulla was opened and a silver-ball electrode was placed on the round window
niche. Electrocochleography was recorded using a SigGen system (Tucker-Davis
Technologies, USA). Clicks (50 µs duration) were presented at a rate of 20/s. Responses
for 500 sweeps were averaged at each intensity level. Threshold was defined as the
minimum intensity that elicited an accurate visible consistent waveform with an
appropriate latency. Compound action potential was measured before vibration
exposure, immediately thereafter, and one, two and three days after vibration exposure.
After the last compound action potential measurement, the animals were perfused
intracardially with physical saline and 4% formalin. Then the bulla was removed, a hole
was drilled on the apex, stapes was removed and the round window membrane was
penetrated to fill the inner ear with fixative. The cochlea was fixed with 4% formalin for
44
12 hours. Vibration and hearing measurements were made by two researchers (the
author and the ear-nose-throat- specialist Jing Zou), in Karolinska Institute.
4.8.3 Analysis of cytokines with immunohistochemistry
(V) For sectioning with immunohistochemistry, the formalin fixed bulla was rinsed in
0.1 mol/L, pH 7.4 phosphate buffer saline (PBS) and decalcified with 0.1 mol/L
ethylenediaminetetraacetic acid-Na2 (EDTA-Na2) for about 6 weeks at 4˚C. After a
rinse in the same PBS, the cochlea was embedded in paraffin and sectioned for 4 µm
thick slices. The sections were deparaffined in xylene for 5 minutes; then placed in
water through a gradationally decreased concentration of alcohol; rinsed in PBS for 2
min; treated with 0.1% trypsin at 37˚C for 10 min; treated with 0.3% Triton X-100 for
3-6 min; rinsed in PBS for 2 min; quenched in methanol peroxide mixture (5 ml 30%
peroxide in 45 ml methanol) for 5 min; rinsed in PBS twice for 2 min each time;
incubated with mouse monoclonal antibody against VEGF receptor 1 and receptor 2
(Sigma, USA), and TNF receptor 1 (Santa Cruz Biotechnology, Inc, USA), or goat
polyclonal antibody against VEGF (Sigma, USA), TNF-α and TNF-α receptor 2 (Santa
Cruz Biotechnology, Inc, USA) (1:2000 diluted in 1% bovine serum albumin, BSA) for
60 min (room temperature, likewise for all the following incubations); rinsed in PBS 3
times for 2 min each time; incubated with normal goat/mouse serum (1:20 dilution) for
15 min; incubated with biotinated goat anti-mouse IgG/mouse anti-goat IgG (1:20
diluted in 1% BSA) for 30 min; rinsed in PBS 3 times for 2 min each time; incubated
with ExtrAvidin-peroxidase (1:20 diluted in 1% BSA) for 30 min; rinsed in PBS 3 times
for 2 min each time; incubated with aminoethyl carbazole for 5-10 min; rinsed in pure
water for 2 min; mounted in glycerine/gelatine. For the negative control, the primary
antibody was replaced by PBS.
For surface preparation with immunohistochemistry, the formalin fixed bulla was
dissected in PBS under the stereomicroscope to remove the bony cochlear shell and
rinsed in PBS 4 more times for 2 min each time. The dissected cochlea was treated with
0.3% Triton X-100 for 3-6 min; then rinsed in PBS 4 times for 2 min each time;
quenched as above; rinsed in PBS twice for 2 min each time; incubated with mouse
monoclonal antibody against VEGF receptor 1 and receptor 2 or goat polyclonal
antibody against VEGF (1:2000 diluted in 1% bovine serum albumin) for 60 min; rinsed
in PBS 5 times for 2 min each time; incubated with normal goat/mouse serum (1:20
dilution) for 15 min; incubated with biotinated mouse anti-goat IgG (1:20 diluted in 1%
BSA) for 30 min; rinsed in PBS 5 times for 2 min; incubated with ExtrAvidin-
peroxidase (1:20 diluted in 1% bovine serum albumin) for 30 min; rinsed in PBS 5
times for 2 min; incubated with aminoethyl carbazole for 5-10 min; rinsed in pure water
for 2 min and the basilar membrane was removed and cut into 6-8 pieces; then mounted
in glycerine/PBS and sealed with nail polish. For the negative control, the primary
antibody was replaced by PBS.
45
4.9 Statistics
The results were measured in following ways:
(I) The results were expressed as means and standard deviations or confidence
intervals. For comparing groups, Pearson crosstabs, Fischer‟s exact test, T-test, or
variance analysis was used. In comparing data, logistic linear or logistic binary
regression was used. Independent variables were included either as continuous or
categorical variables. When probability was less than 0.05 the statement was
statistically significant.
(II) Descriptive statistics and Pearson product moment correlations were calculated for
the continuous variables. Contingency tables were constructed for selected symptom
reports (categorical variables). The symptoms reported by the forest workers, as
confirmed by the examining physician, were taken to be the “gold standard” (i.e.,
assumed correct), and the ability of the observed threshold shifts, expressed per subject
(i.e, four fingers combined), to predict the presence or absence of a symptom has been
estimated by calculating the sensitivity, specificity, positive predictive value, and false
positive rate.
(III) Non-parametric test (Mann-Whitney U-test) and logistic regression were used.
(IV) Descriptive statistics and Pearson product moment correlations were calculated
for the continuous variables.
(V) Nonparametric statistics were used (Friedman‟s test). (Altman 1991).
46
5 RESULTS
5.1 Hand-arm vibration syndrome with use of anti-vibration chain saws: 19-year follow-up study of forestry workers (I)
5.1.1 Cross-sectional study
Cross-sectional studies of Finnish forestry workers were made in 1976-1995, i.e. in a
19-year period, in connection of a compulsory occupational health examination. The
number of workers varied from 109 to 205, and 52 workers took part in all
examinations. The HAVS and musculoskeletal symptoms of the forestry workers are
shown in table 8.
Table 8. Outcome of cross-sectional studies in different years
Year 1976 1981 1986 1990 1995
Number 205 187 183 124 109
VWF (%) 13 4 3 5 4
Numbness (%) 39 55 9 22 28
Pain (%) 26 31 12 22 26
Muscle weakness (%) 11 16 4 6 7
Table 8 key:
VWF = active vibration-induced white finger syndrome
numbness = numbness in the upper extremities
pain = pain in the upper extremities
muscle weakness = subjective hand muscle weakness
5.1.2 19-year-cohort
5.1.2.1 VWF and other symptoms
In the cohort 9 out of 52 forestry workers had active, and 7 forestry workers inactive,
VWF in 1976. In 1995 only 4 forestry workers had active, and 13 had inactive, VWF.
There was one new case after the year 1990. In the cohort, 55% of the forestry workers
were non-smokers, 15% had stopped smoking and 30% were smokers.
47
Table 9. Chain sawing and vibration energy in the cohort in 1995.
VWF N Mean SD SE mean
Chain sawing 0 35 201.4 42.4 7.2
1 17 246.0 38.5 9.3
Vibration energy 0 35 181026.5 67975.5 11490.0
1 17 219814.9 57922.0 14048.1
Table 10.
Levene's Test
for Equality
of Variances
Variances F Sig. Sig.(2-
tailed)
Mean
Differenc
e
SE
difference
95% CI of the
Difference
Lower Upper
Chain
sawing
Equal
variances
assumed
0.508 0.479 0.001 -44.6 12,2 -69.1 -20.2
Equal
variances
not assumed
0.001 -44.6 11,8 -68.6 -20.7
Vibration
Energy
Equal
variances
assumed
1.536 0.221 0.049 -38788.4 19194,4 -77341.6 -235.3
Equal
variances
not assumed
0.039 -38788,4 18148.5 -75567.1 -2009.7
In the cohort, the mean sawing time in 1995 was 246 hours times 100 versus 201
hours times 100. The right grip force was 42 (SD 7) versus 47 (SD 7) kg in VWF versus
non-VWF groups.
The mean sawing time (p=0.001) and right grip force (p=0.038), as measured by
Jamar, differed significantly between VWF and non-VWF groups. VWF was associated
with pain in the upper extremities (Pearson χ2, p= 0.000) and subjective hand muscle
weakness (χ2, p=0.002). VWF and numbness were not significantly associated, but there
was a trend (χ2, p= 0.059). The lifelong vibration energy exposure differed significantly
between the VWF and non-VWF groups ( p=0.001).
48
Table 11. Numbness* VWF 0-1 Crosstabulation
VWF 0-1
Total 0 1
Numbness 0 24 7 31
1 11 10 21
Total 35 17 52
Table 11 key.
VWF= vibration white finger
5.1.2.2 Numbness
The prevalence of numbness in the cohort ranged from 23% in 1976 to 40% in 1995.
Numbness significantly differed between the years 1976-1995 (n= 0.049): 4/52 (8%) of
men had less numbness and 13/52 (25%) of men had more numbness in 1995 when
compared with the year 1976.
Table 12. Pain * Numbness Crosstabulation
Numbness Total
0 1
Pain 0 26 8 34
1 4 13 17
Total 30 21 51
Table 12 key.
Pain= upper extremity pain
Numbness= numbness in upper exremities
Value df
Asymp.
Sig. (2-
sided)
Pearson χ2 13.1 1 0.000
Waking because of numbness was more usual in 1995 than 19 years before (p=0.045).
Numbness was associated with right rotator cuff syndrome and epicondylitis: 7/10 of
rotator cuff patients had numbness (p=0.034) and, also accordingly, 8/9 of right-sided
epicondylitis patients had numbness (p=0.004). Numbness was also associated with the
left-sided epicondylitis (p=0.010).
49
Table 13. Outcome of the cohort study in different years
Cohort (n=52) 1976 1980 1986 1995
VWF (%) 17 6 6 8
Numbness (%) 23 44 40 40
Pain (%) 14 21 27 33
Muscle weakness (%) 2 10 6 10
Table 13 key:
n = number of forestry workers
VWF = active vibration-induced white finger syndrome
numbness = numbness in the upper extremities
pain = pain in the upper extremities
muscle weakness = subjective hand muscle weakness
5.1.2.3 Pain in the upper extremities and muscle force
Rotator cuff syndrome was diagnosed in 19% of 52 men in the right extremity and in
14 % in the left extremity. 17% of forestry workers had epicondylitis on the right. The
diagnoses of rotator cuff syndrome and epicondylitis were found to be associated with
the subjective upper extremity pain during the previous 12 months. Five forestry
workers reported hand muscle weakness in 1995. When measured by Jamar, right hand
grip force was 45.1 (SD 7.3) and left grip force 44.5 (SD 7.9) kg in 1995. The right-
sided upper extremity static functional test (mean 3.75 SD 1.5) did not associate with
rotator cuff syndrome (p=0.643) nor the right-sided dynamic (mean 3.00 SD 1.5) test
(p= 0.577) with rotator cuff syndrome. In the static test, the mean score of the 52 men
was 3.98 (SD 1.5) and in the dynamic test, 3.28 (SD1.4) and 3.19 (1.3), in the right and
left, respectively, in the cohort. These results equated to the average population values.
5.1.2.4 Regional neck pain
In the physical examination regional neck pain (i.e. TN pain) was diagnosed with 38%
of patients. Regional neck pain was associated with numbness (p=0.004), subjective
hand muscle weakness (p=0.003) and pain in the upper extremities (p=0.043). In groups
without or with regional neck pain there was a significant difference in VAS of low
back pain, 20.1 (SD 15.6) mm and 33.9 (SD 22.1) mm, respectively. There also was a
difference in the Oswestry index 8.9 (SD 7.8) versus 16.5 (SD 9.0) indicating disability,
respectively in groups without or with regional neck pain.
50
5.1.2.5 Modelling
The odds ratio of having VWF increased by 3% per each unit of lifelong vibration
energy dose (106 m
2 s
-4 hd). The smokers had a 7-fold odds ratio of having VWF
compared to the non-smokers.
Table 14. Multivariate analysis of VWF in the cohort.
B S.E. Sig. OR 95% C.I.for OR
Lower Upper
Vibrationenergy 0.029 0.009 0.001 1,03 1.01 1.05
Smoking 012 0.025
Smoking 012 (1) -1.582 1.361 0.245 0.21 0.01 2.96
Smoking 012 (2) 1.997 0.985 0.043 7.36 1.07 50.76
Age 0.025 0.076 0.741 1.02 0.88 1.19
Constant -5.179 3.763 0.169 0.01
Table 14 key.
Variable of smoking: 0=no smoking, 1=stopped, 2=smoking
The modeling of numbness in 1995 is shown in table 15. Lifelong vibration energy
did not explain the numbness. Multivariate analysis model including age-adjusted pain
in upper extremities and TN pain could explain 42% of variation in numbness.
Table 15. Multivariate analysis of numbness in the cohort.
B S.E. Sig. OR 95% C.I.for OR
Lower Upper
Vibrationenergy -
0.006
0.007 0.364 0.99 0.98 1.01
Pain 2.520 0.834 0.003 12.43 2.42 63.80
Tension neck 1.787 0.796 0.025 5.97 1.26 28.39
Age -
0.032
0.071 0.654 0.97 0.84 1.11
Constant 0.073 3.400 0.983 1.08
Table 15 key.
Pain= pain in the upper extremities
In a multivariate analysis, both age and lifelong vibration energy modeled right rotator
cuff syndrome. Modeling could explain 69% of variability of right rotator cuff
syndrome. Body-mass index and smoking did not explain rotator cuff syndrome.
51
Table 16. Multivariate analysis of diagnosed right rotator cuff syndrome in the
cohort.
p-value Age-adjusted OR 95% C.I.for OR
Lower Upper
Lifelong vibration energy 0.032 1.04 1.00 1.07
Body-mass index 0.440 1.13 0.82 1.56
Smoking 0.167 9.54 0.39 233.37
5.2 Application of metrics constructed from vibrotactile threshold to the assessment of tactile sensory changes in the hands (II)
5.2.1 Summed normalized threshold shifts
Almost 20% of the Suomussalmi forest workers employed by the National Board of
Forestry were recruited into the study (23 out of 124 persons). Eighteen of the twenty-
three members of this subgroup (78%) attended the compulsory medical examination
almost five years later and agreed to continue to participate. Data for these eighteen
male subjects are presented here.
Table 17. Summed normalized shifts in threshold from expected values, at follow-
up (expressed in units of standard deviations, see equation 1 in chapter 4.5.3.)
Subject Left hand Right hand
Digit 3 Digit 5 Digit 3 Digit 5
1 7.1 8.0 7.0 7.1
2 3.5 0.0 1.9 -1.8
3 2.9 2.2 4.8 5.2
4 3.8 3.4 2.2 3.2
5 2.9 1.9 1.9 4.3
6 1.3 1.0 1.0 2.4
7 2.3 -0.3 -0.8 -1.8
8 3.4 3.3 0.1 2.7
9 -0.3 -1.1 -0.1 -0.2
52
Subject Left hand Right hand
Digit 3 Digit 5 Digit 3 Digit 5
10 2.5 1.1 -0.3 -0.4
11 2.6 3.3 2.4 2.0
12 -0.5 -2.3 2.3 3.5
13 6.1 9.6 7.9 7.7
14 4.4 4.8 4.2 4.0
15 3.0 3.9 4.2 4.8
16 1.8 2.1 2.9 3.1
17 5.2 6.5 4.6 4.6
18 4.5 4.6 4.8 5.2
An inspection of table 17 shows that the majority of summed normalized threshold
shifts are positive rather than negative, implying that the thresholds are, on average, less
sensitive in this group of workers than those to be expected from persons of similar age
engaged in either professional or manual work. See table 18: the individual values were
compared with the boundaries for summed normalized threshold shifts
Table 18. Boundaries for summed normalized threshold shifts and summed
threshold changes
Digit Summed normalized threshold shift Summed threshold change
between studies
Boundary (dB) Boundary
N – A A - AA AA – AAA (dB)
LH3 3.78 5.42 6.76 7.22
LH5 3.88 5.56 6.93 7.92
RH3 3.86 5.54 6.90 7.75
RH5 3.78 5.42 6.76 7.67
Table 18 key: LH= left hand, RH= right hand, 3= finger 3, 5= finger 5
N-A: marginal threshold shift boundary, A-AA: abnormal threshold shift boundary,
AA-AAA very abnormal threshold shift boundary
Statistically significant shifts in threshold were observed in the hands of four of the
eighteen subjects at inception (5/36 hands, or 14%), and of nine of the eighteen subjects
(14/36 hands, or 39%) at follow-up. Significantly, only one hand was considered to
have possessed abnormal sensitivity at the inception of the study, that is, with thresholds
53
rated as AA or AAA (RH of subject #5), while a total of 5/36 hands (14%) possessed
abnormal sensitivity approximately five years later at follow-up. Note that thresholds
judged abnormal are reduced in sensitivity by, on average, more than three SDs from
the mean thresholds recorded in the hands of healthy persons. The probability of such
threshold shifts being found in 'healthy' hands is p < 0.0025. Summed threshold changes
(see equation 5 in chapter 4.5.3.) in sensitivity during the time interval between studies
were recorded in sixteen of the eighteen subjects (25/36 hands, or 70%) (p < 0.005), see
table 19. Of these, twenty hands were assessed to be deteriorating, and four improving
(one hand gave conflicting results).
5.2.2 Summed normalized threshold changes
Table 19. Summed changes in threshold TCSUM between studies, in dB (see
equation 5 in chapter 4.5.3.)
Subject Left hand: TCSUM Right hand: TCSUM
Digit 3 Digit 5 Digit 3 Digit 5
1 23.0 22.2 21.4 21.8
2 9.9 -11.5 2.9 -10.2
3 5.5 -4.6 7.1 12.2
4 13.7 M 7.6 M
5 -9.6 -8.6 -19.3 -9.3
6 4.1 25.6 12.0 9.1
7 6.2 1.0 -10.1 -10.6
8 16.3 13.4 -3.9 6.3
9 10.5 2.8 4.8 6.6
10 6.3 R 6.1 -3.7
11 3.0 8.6 7.4 3.6
12 14.5 M 13.0 M
13 20.9 34.0 35.4 19.1
14 4.9 1.9 6.6 3.8
15 16.5 19.3 18.6 22.8
16 4.2 4.4 4.4 15.7
17 13.0 22.3 18.3 14.3
18 20.8 21.9 10.8 7.0
Table 19 key: R - data rejected; M - data missing. Positive values mean deterioration and
negative values mean improvement of VPT.
54
5.2.3 The correlations between the threshold metrics, age and grip force
The correlations between the threshold metrics, age and grip force are shown in table
20. The thresholds shifts and maximum grip forces are those recorded at follow-up.
Inspection of the correlations in table 16 reveals that the summed normalized threshold
shifts and threshold changes for the SAI and FAI receptors within the fingers on the
right, or left, hand are closely related. The Pearson correlation coefficients of the
threshold shifts were 0.87 and 0.90 for the right and left hands, respectively (p <
0.0005), and 0.79 and 0.67 for the right and left hand, respectively, for the threshold
change.
Threshold shifts occurring in right and left hands are not correlated with the maximum
grip force. The summed normalized TS (i.e. finger with larger TS, worse hand) and the
summed threshold change are not related to age. The maximum grip force and age are
negatively correlated with both hands, as might be expected.
Table 20. Correlations between threshold metrics, age and grip force
Correlation between: By Hand By Subject
TSSum(SD) of digits 3 and 5 (RH) 0.87***
TSSum(SD) of digits 3 and 5 (LH) 0.90***
TCSum of digits 3 and 5 (RH) 0.79***
TCSum of digits 3 and 5 (LH) 0.67*
TSSum(SD) and Grip Force (RH) -0.10
TSSum(SD) and Grip Force (LH) 0.00
TSSum(SD) and age 0.20
TCSum and age -0.12
Age and Grip Force (RH) -0.51*
Age and Grip Force (LH) -0.41
*p < 0.05; ** p < 0.005; *** p < 0.0005
Table 20 key:
TSSUM(SD)= summed normalized threshold shift
TCSUM= summed threshold change
RH= right hand
LH= left hand
55
5.2.4 Prediction of numbness from summed normalized threshold shift
The ability of the measured threshold shifts to predict the presence or absence of
numbness in the hands was examined by forming contingency tables. The threshold
metric was again the summed normalized threshold shift constructed for each subject
(i.e., finger with larger threshold shift, worse hand). The positive predictive value of the
metric was 71% and the false positive rate 18%, when the presence or absence of the
symptom was defined by the boundary between „normal‟ and „marginal‟ acuity. These
values were associated with a sensitivity of 83% and specificity of 82%.
5.3 Postural stability, neck proprioception and tension neck. (III)
TN- patients were compared with subjects without TN (non-TN group). When the
neck muscles were vibrated, the TN- group manifested greater maximum lateral
deviation of position after the first and second stimulation and also a greater average
deviation of position in anteroposterior direction during the second stimulation.
When the lumbar muscles were stimulated, the TN-group showed greater maximum
deviation of position in lateral direction after both the first and second stimulation. The
TN-group had also greater anteroposterior deviation of position after the second
stimulation.
Figure 5. Postural stability of subjects with/without TN
Figure 5 key (neck stimulation):
YM1AFT = lateral deviation of position after first stimulation of neck muscles
XA2 = average anteroposterior deviation of position during second stimulation of
neck muscles and YM2 = lateral deviation of position during second stimulation of neck
muscles.
56
Fig. 6 key (lumbar stimulation):
XMBASE = baseline deviation of position (without stimulation)
YM1 AFTA= lateral deviation of position after first stimulation of lumbar muscles
XM2AFT = anteroposterior deviation of position after the second stimulation of
lumbar muscles
YM2AFT = lateral deviation of position after second stimulation of lumbar muscles
During the calf muscle vibration, the sway in TN was only slightly increased during or
after the vibration stimulation. The sway velocity did not differ after neck, lumbar or
calf vibration stimulation in TN and non-TN groups.
5.4 Vibration-induced hearing loss: mechanical and physiological aspects (IV)
5.4.1 Transfer factor
When comparing the excitation acceleration at different frequencies, the transmission
was significantly better at lower frequencies (32-125 Hz) when compared with higher
Figure 6. Postural stability of subjects with /without TN
57
frequencies (250-1,000 Hz). This relationship is demonstrated in Figure 7 by repeating
vibration at different excitation frequencies. We found no significant resonance
frequencies in the skull. The coupling factor demonstrating transmission of vibration at
different frequencies were: at 32 Hz 0.45 at 63 Hz 0.32, at 125 Hz 0.45, at 250 Hz 0.08,
at 500 Hz 0.05, at 1 kHz 0.01.
5.4.2 Threshold shift immediately following vibration
5.4.2.1 Threshold shift of hearing as a function of vibration frequency
Different vibration frequencies had somewhat different effects on TS. Average TS
(mean of all ABR frequencies) immediately after vibration, as a function of vibration
frequency, were 2 dB (32Hz), 6 dB (63Hz), 8 dB (125Hz), 6 dB (250Hz), 14 dB
(500Hz) and 18 dB (1000Hz). Generally, the higher vibration frequencies (500 through
1000Hz) produced more severe TS than did the lower- mid frequency vibration (32 Hz
through 250 Hz) (p<0.05).
The figure 8 shows the average TS immediately following vibration (at individual
ABR tone burst frequencies) as a function of vibration frequency at 500 Hz.
Figure 7. Transmission of vibration as a function of vibration
frequency
58
555555N =
Tone burst frequency (kHz)
1684210.5
AB
R t
hre
sho
ld s
hift
aft
er
vib
ratio
n (
dB
)
50
40
30
20
10
0
-10
Figure 8. Threshold shift of hearing as a function of vibration frequency at 500 Hz
5.4.2.2 Threshold shift as a function of ABR frequency
All the vibration experiments were pooled. From these experiments, TS as a function
of ABR frequencies 0.5 kHz- 16 kHz were studied. The TSs were greater for ABR
frequencies 4-16 kHz than for the lower ABR frequencies (0.5 to 2 kHz). High-
frequency hearing loss was a typical feature irrespective of vibration frequency
immediately after vibration.
Vulnerability of hearing caused by vibration was modeled. In statistical analysis there
was an interaction between vibration frequency and TS frequency. In modeling the TS,
the vibration frequency was a significant variable (p< 0.001, OR 3.0, 95% CI 2.3-3.7)
and the frequency of ABR was also significant (p< 0.002, OR 1.1, 95% CI 0.4-1.2).
This model could explain 31.5 % of TS variation immediately after vibration (-6.0+ 3.0∙
vibration exposure + 1.1∙ tone burst frequency).
5.4.3 Recovery after vibration
Seven days after vibration, the average TS was nearly recovered to baseline
thresholds. Fourteen days after vibration, recovery was even closer to the baseline
measurements.
59
Immediately after vibration TS was at least 10 dB (ranging from 0 to 40) at two ABR
frequencies in 60 % (18 / 30) of the animals. At day 7 the TS was at least 10 dB at 2
frequencies in 3 animals, and at day 14 in 4 animals, respectively. Average TS over all
frequencies was 8.8 dB immediately after vibration exposure, 2.4 dB at day 7 and 1.3
dB at day 14. Vibration frequency was still a significant determinant for recovery (p<
0.01, OR 0.6, 95% CI 0.1-1.0) in modeling the TS at day 7.
5.5 Vibration induced hearing loss in guinea pig cochlea: Expression of TNF-alpha and VEGF (V)
5.5.1 Expression pattern of TNF-α in the vibration stimulated cochlea
No TNF-α expression was detected in the normal cochlea. Vibration induced TNF-α
expression appeared mainly in the reticular lamina, the bottom of the outer hair cells,
Deiters‟ cells, Hensen‟s cells, Claudius cells, the internal sulcus cells, the spiral
ligament, the spiral vascular prominence and the cochlear vasculature.
5.5.2 Expression pattern of TNF receptors in the vibration stimulated
cochlea
After vibration, a weak TNF receptor 1 staining was found mainly in Hensen‟s cells,
Claudius cells, the internal sulcus cells and the capillaries of the spiral ganglion. Much
stronger expression of TNF receptor 2 was found mainly in the spiral ganglion cells,
Hensen‟s cells, Claudius cells, the internal sulcus cells, Deiters‟ cells, the basal
membrane of the organ of Corti, the spiral ligament, the spiral vascular prominence. A
Figure 9. TNF-α in the vibrated cochlea
Figure 9
Strong expression exists in
the organ of Corti (), Border
cell (), Claudius cell (),
interdental cell, the spiral
ligament () and the cochlear
vasculature ()
60
weaker staining was found in the bottom of the outer hair cell. No TNF receptor
expression was detected in the normal cochlea.
5.5.3 Expression pattern of VEGF in the vibration stimulated cochlea
No VEGF expression was detected in the normal cochlea. In the vibrated cochlea,
VEGF was detected in the stereocilia of the inner hair cells and the outer hair cells and
supporting cells (figure 10). Especially the spiral ganglion cells, Deiters‟ cells, Hensen‟s
cells, Claudius cells and the internal sulcus cells were stained. No expression of VEGF
was detected in stria vascularis.
Figure 10. VEGF expression in the vibrated cochlea shown by surface preparation and
immunohistochemistry. Strong expression was detected in the stereocilia () of the
IHC and OHC, and the supporting cells () (400×);
5.5.4 Expression pattern of VEGF receptors in the vibration stimulated
cochlea
No VEGF receptor 1 or 2 expression was found in the normal cochlea. VEGF receptor
1 was not detected in the vibrated cochlea, whereas VEGF receptor 2 expression was
present in the bottom of the outer hair cells, Deiters‟ cells, Hensen‟s cells, Claudius
cells, the basal membrane of the organ of Corti, the internal sulcus cells, nucleus of the
spiral ganglion cells, the lateral wall of scala tympani and the spiral ligament (figure
11). No expression of VEGF receptor 2 was observed in stria vascularis.
Figure 10. VEGF expression in vibrated
cochlea
61
c. d.
Figure 11a. (left) VEGF R2 expression in the vibrated cochlea. a strong expression is
in Hensen's cell (), Claudius cell () Border cell (), weak expression in the spiral
ligament () (200×).
Figure 11b. (right) Weak expression was detected in the spiral ganglion cell ().
5.5.5 Hearing loss after vibration
The average hearing loss after vibration was 62 dB (SD 35 dB). One animal became
deaf. We observed a tendency for recovery so that in day 4 the mean hearing threshold
was 48 dB but the difference was not statistically significant (Friedman‟s test, p=0.175).
Figure 11a and b. VEGF R2 expression in vibrated cochlea
62
6 DISCUSSION
In this clinical and experimental study the biological responses to vibration were
evaluated. The aim was to evaluate the clinical responses among forest workers and
then, in experimental study, to evaluate the vibration responses using inner ear as a
model organ. In this model organ all the important elements as vascular structures,
sensory cells, and nerves can be studied. Furthermore the methods to evaluate
physiological responses and anatomical changes are relatively well developed for the
inner ear.
6.1 Methodological aspects
A part of this study was was longitudinal and the data of the forestry workers in
Suomussalmi was collected over a 19 year period. The attrition rate during the years
was high as it is common in longitudinal studies running for decades. In a previous
study, Koskimies (1992) found that the decrease of VWF occurred mainly through the
technical development of the anti-vibration chain saws, the warm transport, the
protective clothing and the improved occupational health care among these forestry
workers. This study confirmed the trend toward the diminution of the prevalence of
VWF (Koskimies et al. 1992). However, the sample size of VWF in current study was
small. For epidemiological studies, the amount of the symptomatic population should be
larger. Further studies should evaluate the connection of the ergonomics with the
vibration exposure.
The measurements of VPT showed a good repeatability. VPT discriminated subjects
with severe symptoms of HAVS. The statistical associations between threshold shifts
and threshold changes in digits 3 and 5 of the same hand (table 16) suggest that in
modeling the vibration damages in VPT it is advisable to consider the vibrotactile
effects rather by hand than by finger. The ability of the threshold shifts to predict the
numbness reported by the forest workers shows that this metric is closely associated
with the tactile sensory changes occurring in the hands of these subjects. VPT can be
used as a screening method, but it still needs validation of measurements. There are
different types of VPT measurements in use, which makes comparison between studies
difficult.
With the force platform, the accuracy was mainly limited by the initial calibration that
was made before every measurement. The testing with eyes closed may affect more the
oldest of the group than the younger ones in general, but it may not bias the result. The
most pronounced deviation of position was found during the neck and lumbar area
stimulation, not during the stimulation of calf muscles. The muscles in neck area are
important in proprioceptive control of balance.
When comparing the vibration level of burr to the vibration of the experimental set-up
in the animal model it must be noted that the measured values in burrs used in temporal
bone surgery are not evaluated in a comparable way. The dominant frequencies of the
63
vibration level are not indicated in the literature. The nominal speed of the drill will be
reduced during work as the drill is compressed to the bone to allow better cutting of the
bone. In these circumstances the speed of drill will range around 125 to 250 Hz as in the
present experiments. The size of the skull in guinea pig is much smaller than in man and
thus the vibration is transmitted more easily into the animal cochlea than in a human.
When evaluating the level of noise generated by the drill in the middle ear, the noise
level in the guinea pig was 108 dB which is similar to that reported in clinical papers.
In the instrumentation set-up described in this paper there was some non-linearity in
coupling of vibration to the skull. The non-linearity indicates a variation of contact
between the shaft and the skull. This may lead to reduced vibration or to impulsive
excitation. If the characteristics of the skull vibration would become non-linear, the
amplitude response could not be calculated from the excitation magnitude. In these
cases the measurement repeatability would be poor. The linearity measurement showed
that the used amplitudes were at the expected linearity range. Nevertheless, we observed
at the low frequencies (32-125 Hz) decoupling in the transmission of vibration from
vibrating shaft to the skull. This variation, although minor, seems to be linked to the
inherent characteristics of the vibrator system rather than the skull resonances. In the
guinea pig skull no definite resonances were found when using sinusoidal sweep. The
behaviour of guinea pig skull is much the same as reported in human (Bekesy 1932,
Tonndorf 1968).
We analyzed the up-regulation of TNF-α and VEGF in cochlea after 32-1000 Hz
vibration exposure. Both of these factors were found in several cell types in the cochlea
after vibration. Shear stress induced VEGF expression seems to be dependent upon
time. After acute shear stress as within 6 hours from the exposure Gan et al. (2000) did
not found an increased expression; whereas after longer shear stress, its expression is
increased up to 14 days (Milkiewicz et al. 2001). In the cochlea we observed expression
of VEGF and VEGF R2 1-3 days after vibration. This is in accordance with the time
limit of previous reports that protein production in the cellular machinery has a definite
latency. In the guinea pig study described here, we analyzed vibration-induced health
effects. There is a need for further animal studies which utilize a shear stress model
applicable to HAVS.
6.2 Clinical aspects of vibration- induced health hazards
In a 19-year cohort study of Finnish forestry workers we evaluated the occurrence of
symptoms of hand-arm vibration syndrome and musculoskeletal disorders as rotator
cuff syndrome and epicondylitis. Also a dose-response relationship with vibration and
VWF, but not in numbness was demonstrated. There was a significant increase in
numbness in the cohort. The sample sizes of subjects in this study were small, however,
resulting in wide confidence intervals. The study concentrated on the results of the last
year of the cohort. Additional studies are needed in different occupations using
vibrating tools, as the work methods and tools are constantly changing.
In Italian studies, Bovenzi et al. (1995c) found a dose-response relation for vibration-
induced vascular disorders; there was a 51.7% prevalence of VWF in forestry workers
64
who had used both non-AV (antivibration) and AV chain saws and a 13.4% prevalence
of VWF in workers having used only AV chain saws, respectively. In Italy, the use of
AV chainsaws was more recent than in Finland. The difference with Bovenzi‟s results
reflects the difference in lifelong vibration energy exposure, and also differences in
smoking habits. In Bovenzi et al‟s study (1995c), 70.3% of forestry workers were
smokers in comparison to 30% in our study. In our study (I), the weighted acceleration
of the chain saws has stayed in the range of 1.8-2.2 ms-2
since the early 1980‟s. In
Japan, Mirbod et al found VWF symptoms in 9.6% of forestry workers with AV chain
saws which is supportive of our study (Mirbod et al. 1995). The repeated surveys we
used reduced the recall bias of VWF. In our study (I), the diagnosis of VWF was
evaluated by medical history of symptom development and temporal pattern of
symptoms. Earlier the symptoms of these forestry workers were evaluated with cold
provocation tests.
Cigarette smoking is one of the risk factors related to vascular diseases. In this study
(I), we could confirm that smoking is a 7-fold risk factor of VWF. In the cohort 15% of
the men had stopped smoking in 1995, which may bias the result to some extent.
Cherniack et al. (2000) showed that smoking may aggravate digital arterial spasm in
plethysmography.
In the follow-up, we could not find a dose-response with vibration energy and
numbness. There seems to be different pathophysiological mechanisms leading to
sensorineural and vascular changes in vibration-exposed forestry workers (Pelmear
2003, Bovenzi et al. 2000b).
Numbness is connected with vibration-induced neuropathy (Koskimies et al. 1990,
Dasgupta and Harrison 1996, Cederlund et al. 1999, Bovenzi et al. 2000b). In this
cohort (I), numbness varied during the 19 years. In 1983 cross-sectional study,
electroneuromyography was taken from the cohort subgroup, which was randomly
selected. Carpal tunnel syndrome was diagnosed in 20% of forestry workers on the
basis of measurement and clinical data (Koskimies et al. 1990). Numbness was
associated with upper extremity pain in our study (I). On the basis of this cohort, we
cannot make a differentiation between specific neuropathies and unspecific symptom of
numbness. The high prevalence of numbness in our study was exposure-independent. It
confirms the result of Cherniack et al. (2000).
The prevalence of numbness and upper extremity pain varied in the beginning of
the1980‟s mainly because the chain saw operation time increased from 3-4 hours to 4-5
hours. In the same time, the productivity of forestry work increased. In this study, one
third of forestry workers reported upper extremity pain in the cohort, which also
supports other studies (Färkkilä 1978, Mirbod et al. 1995). Subjective pain in the upper
extremities was associated with the shoulder and elbow musculoskeletal disorders.
Right rotator cuff syndrome could be modeled by age and by lifelong vibration energy.
Palmer et al. (2001) also reported increased risk of shoulder pain in the workers with
daily vibration exposure.
Tendons transmit mechanical tension during muscular contraction. Forces that exceed
the capacity of tendon to adapt, for example because of high force or awkward posture,
can result in inflammation and fibrotic changes (MacKinnon and Novak 1997). Rotator
cuff syndrome has a multifactor etiology. The predisposing factor for rotator cuff
syndrome is degeneration, with impairment of circulation and mechanical stress. In
65
addition to vibration exposure, the static loads and extreme postures are the risk factors
in forestry work (Miranda et al. 2001). In our study, rotator cuff disorder was associated
with the vibration exposure in forestry work, although the sample size was small.
The diagnosis “tension neck” was adopted from Waris (1979). It closely resembles the
present diagnosis of non-specific neck pain, cervicalgia (M54.2) in International
Classification of Diseases (ICD-10). In this study, the degree of degeneration by x-ray
was not reported, but degeneration may be a significant factor behind neck pain. It is a
limitation of this study. However, the prevalence of degenerative changes of
intervertebral discs and vertebrae of cervical column is high also in asymptomatic
people (Gore 2001).
Lateral epicondylitis is a condition of pain in the region of lateral epicondylitis,
especially at the origin of extensor carpi radialis levis (Bennett 1994). Epicondylitis was
less common than shoulder disorders, which may be in connection with the
unemployment prior to examination. 18% of forestry workers had epicondylitis on the
right. In previous studies, 29.3% of Italian forestry workers had epicondylitis (Bovenzi
et al. 1991). It is in line with present results.
The pathogenesis of epicondylitis is not fully understood. The main theory is that
microruptures occur at the site of between the insertion of extensor muscles and bone,
causing inflammation and resultant granulation tissue (Coonrad and Hooper 1973,
Leach and Miller 1987) In our study, musculoskeletal investigation was carried out by
two specialists in physical medicine and rehabilitation. There may be interexaminor
differences in diagnosing musculoskeletal disorders, but it should not bias the result,
because the main principles of the clinical examination were agreed together.
Our forestry workers (I-III) were on 6-week unemployment leave prior to
investigation in 1995. Their shoulder and elbow musculoskeletal disorders had time to
recover. The history of shoulder and elbow disorders was carefully taken. In diagnosing
rotator cuff tendinitis, the group of symptom cases of rotator cuff syndrome and the
group with positive provocation test of rotator cuff syndrome (positive painful arch test
during elevation, pain in resisted abduction or resisted external rotation) had to be
combined (i.e. to be the “rotator cuff syndrome” group, refer to chapter 4.3.), for
statistical analysis. Accordingly, also epicondylitis group of symptom cases was
combined with the group of positive provocation test of epicondylitis, for statistical
analysis (to be the “epicondylitis” group). This may have biased the result to some
extent. However, assumingly, many of symptom cases may have had a positive
provocation test earlier, during working months. This unemployment period was
independent of the research.
The functional upper extremity tests were earlier widely used in Finland by
occupational health care. It was assumed that there is a significant difference between
the groups with or without musculoskeletal symptoms. In these studies dynamic and
static muscle force of upper extremities were measured. They did not differentiate
between groups of having or not having rotator cuff syndrome or epicondylitis. Pain in
the upper extremity may interfere with upper extremity test results to some extent and
bias the result. Measurements are not recommended for use as a screening method in
occupational health care.
Subjective deterioration of muscle force occurred in the cohort. In a two-year follow-
up of forestry workers in Finland, Färkkilä et al. (1986) reported a 21% loss of muscle
66
force among subjects with VWF when compared to 5% loss in asymptomatic controls.
Hand muscle weakness was also reported by Bovenzi et al. (1991).
.
6.3 Clinical aspects of sensory threshold changes
In essence, the threshold shifts provide a measure of the status of each finger/nerve
system at inception, and follow-up, for an individual relative to the mean thresholds of
healthy persons, while the threshold changes provide a measure of what has happened
to each finger/nerve system over the five-year period, with each subject serving as his
own control.
The summed normalized threshold shifts tend to follow one of several patterns.
Overall, there is a general elevation in threshold (i.e., positive threshold shift)
corresponding, implicitly, to a reduction in acuity in the hands of this group of forest
workers.
In one pattern, the elevations in threshold of digits 3 and 5 of the same hand tend to be
similar in magnitude. The pattern is often common to both hands. This was more
evident in the data obtained at follow-up (shown in table 13). The results strongly
suggest that there are neurological changes occurring similarly in the nerve fibers and/or
end organs mediating tactile perception at the fingertips of digits 3 and 5 in both hands
of this subject. It may therefore be inferred that both median and ulnar sensory nerve
fibers and/or end organs are affected similarly.
A second pattern, which is uncommon in this group of subjects, is a variation: the
magnitude of the shift differs between the left and right hands of a subject. An example
is provided by the results for subject #3 (table 13).
A third pattern, which is also uncommon in this group of subjects, involves larger
threshold shifts in digit 3 than in digit 5 of the same hand. In this case the inference
would be that the median sensory nerve fibers and/or end organs of digit 3 are more
affected than the ulnar sensory nerve fibers and/or end organs of digit 5 of these hands.
A corresponding fourth pattern involves larger threshold shifts in digit 5 than in digit 3
of the same hand. The interpretation would be the opposite of the third pattern.
Overall, the strongest trend from study inception to follow-up is one of increasing
summed normalized threshold shift. There was one exception. The thresholds of subject
#5 show a marked reduction (i.e., improvement in sensitivity) from 1990 to 1995, which
was coincident with a reduction in alcohol consumption during this period. A small
fiber neuropathy had been detected by electroneuromyography in this subject.
The progression in individual hands is obtained from the summed threshold changes
over the five-year period (table 15). The common trend was one of deteriorating
sensitivity, with summed mean threshold changes of up to 35.4 dB recorded.
Reductions in sensitivity of threshold changes in excess of 20 dB were observed in the
fingers of, in total, eight hands (table 15). Studies of the rate of threshold change with
age in healthy persons (including professional and manual workers) would yield a mean
summed threshold change of TCSUM 0.7 dB due to ageing during the five year period
(Brammer et al. 1993), much less than the magnitude of TCSUM observed in these
subjects.
67
If the thresholds recorded from the three foremen (subjects # 4, 12 and 16) included in
this study (who did not work with power tools) are considered to provide a more
appropriate measure of threshold change over the five year period for the lifestyle and
environment of the Suomussalmi region, then the summed threshold change for persons
not using power tools at work would be TCSUM = 9.7 5.0 (SD) dB, leading to a 95%
confidence interval of 0 < TCSUM < 19.5. While the large confidence interval and small
number of workers from which it was derived may be questioned, the changes in six
subjects still remain statistically significant. Thus, arguably 40% of the remaining
subjects are experiencing work-related threshold changes in their hands, assumingly
caused mainly by vibration.
6.4 Postural stability and neck pain
The diagnosis of TN pain was established with 27 out of 106 the forestry workers. The
cervical spine of one forestry worker had been previously operated, and he had cervical
syndrome with radiating pain. In the cohort (I) the TN pain was associated with
Oswestry index, which reflects the disability from low back pain. Patients with neck
pain had also low back pain. The other Oswestry involving neck symptoms was not
used in this study, which is a restriction. Palmer et al. reported that patients with hand-
arm vibration exposure had an increased risk of neck pain (Palmer et al. 2001) which we
could not confirm.
The patients with TN and without TN had similar postural responses during a
stimulation-free period. Anteroposterior forward shift occurs in neck muscle vibration
in healthy subjects (Pyykkö et al. 1989). In TN patients the average deviation of
position in the anteroposterior direction was greater than in the control group, and also
the lateral maximum deviation of position during the second stimulation.
During the lumbar stimulation, the position shift forward normally occurs. It can be
explained by a general alerting reaction, to achieve a safer position (Pyykkö et al. 1989).
The TN group had greater maximum anteroposterior deviation of position after the
second stimulation. The TN patients also manifested greater lateral maximum deviation
of position after the first and second stimulation. Pain and stiffness in the neck are
common in a working population. Also Karlberg found that patients with chronic
cervico-brachial pain had poorer postural control (Karlberg et al. 1995)
Physical work requires muscle energy. Local metabolic changes in muscle are
conveyed into the brain by sensory afferent nerves and cause sensation of discomfort
and fatigue (Armstrong et al. 1993) Reduced local blood flow in the trapezius correlated
with myalgia and was found in connection of static load at work (Larsson et al. 1990).
In TN the activation or control of afferent nerve endings may be faulty and may lead to
inadequate postural responses.
Low back pain was not taken into account in the TN study. In the cross sectional study
TN pain was associated with low back pain. It is possible, that in this study low back
pain could be involved in postural stability differences, especially during lumbar
vibration stimulation. However, Luoto et al. (1998) found that with vibration
stimulation of back muscles, lateral deviation of position was greater among patients
68
with low back pain, but only when eyes were open, not when they were closed. In our
study, the eyes were closed during measurements
6.5 Inner ear as a model organ for sensorineural damage
Sensorineural hearing loss (SHL) is well known to occur after different acoustic
(vibration and noise induced) traumas, such as middle ear surgery, with an incidence of
up to 5% (Kylen and Arlinger 1976). Postoperative SHL analysed in 2,303 cases of
chronic otitis media showed that 0.5% became totally deaf and 0.7% acquired a high
tone loss (Tos et al. 1984). Using high frequency audiometry of up to 20 kHz, the
incidence of SHL has been recorded in 37.5% of patients (Domenech 1989). The
mechanisms producing sensorineural hearing loss in burr vibration may be similar to
those producing a sensory threshold reduction in the hands of exposed workers
Transcranial vibration represents a complex interaction of transmission and damping
effects of the skull, cranial contents, and surrounding soft tissues. The complex patterns
of vibration transfer across the skull have been investigated with increasing resolution
since Herzog and Krainz (1926), Bekesy (1932) and Barany (1938) who generated early
systematic data on bone conduction (Brandt 1989). Tonndorf (1968) expanded the
treatment of these data to convincingly demonstrate that modes of bone conduction are
frequency dependent. The large amplitude vibration at frequencies less than 200 Hz
results in the skull vibrating as a rigid body, producing a transitory type of motion as
first proposed by Barany (1938). In the transitory mode the cochlear fluids are set in
motion while the ossicular chain is stabilized. The result is differential vibration of
mobile structures and displacement, with activation of cochlear transducers.
As the frequency of stimulation is raised, “flexural-compressive” modes of
stimulation begin to appear (Bekesy 1932, Tonndorf 1968). At higher frequencies the
oscillatory movement is transmitted to the auditory ossicles, and into the cochlea
including ossicles, labyrinths, fluids inside the cochlea, tegmentum and partially the
cochlear nerve. Vibratory energy reaching the cochlea generates segmental
compressions and expansions of the cochlear shell. Compressed cochlear fluids seek
relief by pushing and pulling the oval and round windows. The relatively greater
compliance of the round window facilitates fluid shifts from the scala vestibuli into the
scala tympani, displacing the basilar membrane and cochlear transducers. The mode of
cochlear shearing forces during vibration at higher frequencies might result in greater
vulnerability. The phenomenon is undoubtedly complex and occurs at higher vibration
frequencies and it remains to be documented what role burr vibration exposure may
have in the aetiology of inner ear damage. The mechanics of hand-arm system with
bones and joints represents different system. So far no studies are performed in that the
different tissue compartments of the hand would be modeled in detail. Thus oscillation
of vascular components, connective tissue, and sensory organs may follow the
principles observed in the temporal bone.
Freeman et al. (2000) and Sohmer et al. (2000) presented an interesting theory for
bone conduction in humans and rodents, in that fluid pathways to the inner ear would
cause the major effect of bone conduction (Freeman et al., 2000; Sohmer et al., 2000).
69
Thus, the placement of bone vibrator to the fontanel of an infant or eye or brain tissue
produced equal or better hearing than placement of the bone vibrator on the frontal or
mastoid bone. These experiments are difficult to interpret as a fixing method of the
accelerometer to the bone was not demonstrated and the couplings of skull vibration
with the soft tissue vibration were not demonstrated. These works indicate, however,
that the CSF pathways may significantly modify the bone conduction.
It is well accepted that shear movement exists in the organ of Corti, but no document
has mentioned shear within the spiral ganglion cell. Vibration induced shear forces
within the bone matrix stimulate bone cells and mechanically transform them causing
upregulation of genes in the cells (Turner et al. 1994, Nomura and Takano-Yamamoto
2000). The spiral ganglion cells are surrounded by perilymph and bone matrix. The
shear force produced by the transcranial vibration is conducted to the spiral ganglion
cells and is able to cause shear stress. In our study (V), the strong TNF receptor 2,
VEGF and VEGF receptor 2 gene expressions in the spiral ganglion cells support this
hypothesis.
At the vibration exposure level studied here, most of the TS of hearing was temporary
and recovered within the first week. The clinical findings of temporal bone surgery in
human also demonstrate that patients have a significant high tone hearing loss
immediately after surgery. Vasama demonstrated TS in 55% of patients in exostosis
surgery of the external auditory canal. In 10% of the patients the TS was prominent
(Vasama 2003). Our results (IV) support his findings. In ear surgery it is stated that
mostly the TS recovers within one week, if the level of vibration is not overwhelming
and the frequency of vibration is low (Da Cruz et al. 1997, Tos et al. 1989). We
observed permanent TS (at least 10 dB) in 3 out of 30 animals 7 days after the vibration
exposure, and the average TS was only 2.4 dB. Transmission electron microscopy may
verify any mechanical damage of the organ of Corti. This work is ongoing.
Forestry workers with vibration–induced white finger have aggravated hearing loss
(Pyykkö et al. 1981, 1986c, 1988, 2003). These authors showed that forestry workers
with vibration-induced white fingers (VWF) had about a 10 dB greater TS in hearing
than forestry workers without VWF (Pyykkö 1986c). The relationship between hand-
arm vibration and hearing loss was confirmed only on epidemiological basis (Pyykkö et
al. 1986c, 1988, Starck et al. 1988, Iki et al. 1986), and the mechanism behind the
hearing loss is unknown (as is the mechanism leading to vibration damage in the
tissues). Long-term vibration of hands is known to result in disturbances, especially in
the circulation of hands (Koskimies et al. 1992, Griffin and Bovenzi 2002, Griffin et al.
2003). On the other hand, Palmer et al. (2002) showed that there is an association
between finger blanching and hearing loss, even prior exposure to hand-arm vibration,
possibly through sympathetic vasoconstriction in the cochlea.
In addition to patients exposed to vibration in middle ear surgery, inner ear damage
may occur in persons exposed to whole body vibration such as in tractor driving, stone
work, forestry, helicopters, mining (Zou et al. 2001). These occupations may be at risk
for vulnerability of noise.
70
6.6 Upregulation of the cytokines during vibration exposure
We examined the possibility whether up-regulation of TNF-α and VEGF would be
involved in the hearing loss (V). Although TNF-α, TNF receptor 1 and receptor 2 were
observed in the vibrated cochlea, the expression of TNF receptor 2 was more prominent
in the cochlea. The combination of TNF-α with TNF receptor 2 is capable of activating
Jun N-terminal kinases (JNK) and nuclear factor (NF)-κB (Goeddel 1999). The
activation of JNK and NF-κB has the function of an anti-apoptotic agent (Goeddel
1999, Watanabe et al. 2002, Biswas et al. 2003). On contrary, the activation of TNF
receptor 1 induces apoptosis (Ashkenazi et al. 1998, Goeddel 1999). When both
receptors are expressed, the activation of TNF receptor 2 enhances the effects of
receptor 1 activation. The final fate of the cells should be related to the expression ratio
of both receptors. Shear stress inhibits TNF-α induced apoptosis by activating
phosphatidylinositol 3 (PI3)-kinase and inhibiting Caspase-3 (Pavalko et al. 2002).
Vibration induced VEGF and VEGF R2 expression in the cochlea, but not VEGF R1.
Our results confirm the biological significance of a previous in vitro study, which
indicated that in vascular endothelial cells high shear stress induced an increase in
VEGF R2 expression. This up-regulation reached its maximum and was in a linear
gradient to the stress strength within a range of 2 to 40 dyne/cm2
(Abumiya et al. 2001).
The authors interpreted that an increase in the shear stress in the vasculature by post-
ischemic reperfusion stimulates VEGF R2 expression, resulting in an increase in
vascular permeability and leading to neo-vascularisation. After myocardial infarction
the newly formed myofibroblasts express VEGF and VEGF R2 that seem to play a
significant role in tissue repair/remodelling (Chintalgattu et al. 2003). When the cochlea
is exposed to mechanical vibration, a shear stress is increased in the various cell types
of the cochlea with concomitant increase of expression of VEGF and VEGF R2. Thus,
VEGF may contribute to tissue remodelling and angiogenesis at the site of damage in an
autocrine manner and may be important in preventing further damage to the cochlea.
The mostly enhanced expression was located in the spiral ganglion cells, stereocilia,
supporting cells, the internal sulcus cells and epithelial cells of the lateral wall of the
scala tympani. The spiral ganglion may be repaired under assistance of VEGF because
both VEGF and VEGF R2 were expressed there.
Seki et al. (2001) suggested that the pathophysiology underlying vibration-induced
hearing loss is an increase in porosity of the blood vessels in stria vascularis and
degenerative changes in the intermediate cells of stria vascularis. The exact mechanism
is being investigated. Vibration damage seem to cause upregulation of TNF and
TNFα-receptors in spiral ganglion cells, and may cause necrosis and apoptosis, which
leads to nerve degeneration.
71
7 CONCLUSION
The pathophysiological effects of vibration were studied.
(I) In the cross-sectional study, the prevalence of VWF was reduced and incidence
was very low. The results in the cohort study indicated that in spite of a low prevalence
of VWF (8%), sensorineural symptoms as numbness increased. Numbness was
exposure-independent. Musculoskeletal disorders in the cohort study were more
prominent on the right upper extremity, which carries the weight of the chain saw.
Vibration contributed to the development of musculoskeletal disorders in the upper
extremity of forestry workers.
(II) Two tools have been constructed from mechanoreceptor- specific threshold shifts
and threshold changes to assess tactile sensory function in the hands of forestry
workers. Four patterns of threshold shift could be identified. The most common pattern
in this group of subjects involved both hands and both median and/or ulnar sensory
nerve pathways. Statistically significant positive threshold changes (i.e., reductions in
sensitivity) were recorded in a majority of the hands over a five-year period. The
threshold shift metric is closely associated with the tactile sensory changes.
(III) 27 out of 106 of forestry workers suffered from TN. TN-patients had poorer
postural stability. In TN patients the activation or control of proprioceptive afferent
endings may be faulty and may lead to inadequate postural reflexes. Vestibulospinal
reflexes converge with proprioceptive input. There may be a mismatch of the impulses
in the central control mechanisms.
(IV) In the animal model of the inner ear high frequency vibration causes more injury
than low frequency vibration. The vibration can be exactly dosed and the responses
evaluated with ABR.
(V) In vibration induced hearing loss it seems that shear stress may be the key factor
for up-regulation of TNF-α, VEGF, TNF R1, TNF R2 and VEGF R2. The function of
TNF-α is two-way, it can induce both cell damage and protection against apoptosis. The
function of VEGF is to repair some of the damages to the cochlear cells.
In the future, an approach should be taken to evaluate the role of biomechanical risk
factors in connection with hand-arm vibration exposure. Neurological examination may
require ENMG, VPT and quantitative sensory testing in the future. The validity of the
specific VPT in forestry worker population must be verified.
The inner ear damage model may provide insight into vibration-induced damages in
the hand-arm vibration syndrome. It may provide a new understanding of mechanisms
leading to vibration-induced hearing loss and vibration-induced cellular damage. In the
future, detailed mechanism of vibration induced SNHL and pathophysiological
mechanisms leading to HAVS should be researched.
More studies are needed for estimating the dose response relationship of vibration and
SNHL in this model. Additional studies on upregulation of cytokines involved in the
apoptotic pathway, in addition to TNF-α, are suggested. Also, the studies with the
electron microscopy, magnetic resonance imaging and atomic force microscopy are
needed to evaluate structural changes in cellular and molecular level in the inner ear.
72
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9 ORIGINAL PUBLICATIONS
I. Sutinen P, Toppila E, Starck J, Brammer A, Zou J, Pyykkö I. Hand-arm
vibration syndrome with use of anti-vibration chain saws: 19-year follow-up
study of forestry workers. Int Arch Occup Environ Health 2006; 79(8): 665-71.
II. Brammer AJ, Sutinen P, Diva UA, Pyykkö I, Toppila E, Starck J. Application of
metrics constructed from vibrotactile threshold to the assessment of tactile
sensory changes in the hands. Submitted for publication (Journal of the Acoustic
Society)
III. Koskimies K, Sutinen P, Aalto H, Starck J, Toppila E, Hirvonen T, Kaksonen R,
Ishizaki H, Alaranta H, Pyykkö I. Postural stability, neck proprioception and
tension neck. Acta Oto-Laryngol Suppl 1997;529:95-7
IV. Sutinen P, Zou J, Hunter LL, Toppila E, Pyykkö I. Vibration-induced hearing-
loss: mechanical and physiological aspects. Otol Neurotol 2007; 28(2): 171-7.
V. Zou J, Pyykkö I, Sutinen P, Toppila E. Vibration induced hearing loss in guinea
pig cochlea: expression of TNF-alpha and VEGF. Hear Res 2005; 202(1-2):13-
20.
Appendix I
HAASTATTELUKAAVAKE Suomussalmella (metsuritutkimus)
Päivä
Anamneesi: Nimi: Syntymäaika:
Herediteetti TVD (eli VWF): on/ei
Lapsuus tai loppunut
Kouluikä
Sotaväki
Ensi käynti lääkärillä: Dg: 1.
Minkä vuoksi: 2.
3.
1. TVD (eli VWF) alkanut: oik/vas viim.kohtaus:
kohtauksen kesto (metsässä):
muutos: lieventynyt/ennallaan/vaikeutunut
esiintyminen: työmatkoilla/tauoilla/sahatessa/aamulla/iltapäivällä/muu,mikä
paikallistuminen käteen
Paikallistuminen käteen (Vasen)
Paikallistuminen käteen (Oikea)
Muutos:lieventynyt/
ennallaan/
vaikeutunut
Sää:kuiva pakkanen/ kostea 0-sää/ myös kesällä/ muu,mikä:
Kohtausten lukumäärä viikossa: <1/ ja muutos: lieventynyt/ennallaan/ vaikeutunut
1-4/
>4
2. Puutuminen tai kipu yläraajoissa:
kyllä/ei
päivällä herää/ yöllä/ muulloin
ei herää/ kerran viikossa/ 2-6 kertaa viikossa/ joka yö/ useammin
3. Puristusvoiman heikkeneminen
kyllä/ei
oikea/vasen
muutos: lieventynyt/ ennellaan/ vaikeutunut
4.Nivelsärky
kyllä/ei
oikea: sormet, ranteet, kyynärpää ja olkapää/ kokovyläraaja
muutos: lieventynyt/ ennellaan/ vaikeutunut
5. Muuta
RR oik/vas
La Hb Virtsa
Cor Pulm EKG:
6. Moottorisahahaastattelu
oireet:
totaalisahausmäärä (tunneissa)
Muut tärisevät työkalut:
Appendix II
INTERVIEW (TRANSLATED by the author of the thesis)
Date
Medical history Name Date of birth:
Heredity TVD (or VWF):
Childhood yes/ no/ ended
Schoolyears:
Army
First visit to a doctor: Diagnosis: 1.
The reason: 2.
3.
1.TVD (or VWF) alkanut: right/left Last attack
the duration of the attack:
change: improved/ the same as before/ deteriorated
occurence: during the transfer/ brakes/ chainsawing/ in the morning/ in the afternoon/
other, what:
localization in the hands:
change: improved/ the same as before/ deteriorated
The left hand
The right hand
Change: improved/
the same as before/
deteriorated
Weather: dry subzero weather/ damp zero weather/ also in summer/ other, what:
The amount of attacks in a week: <1/
1-4/
>4
and change: improved/ the same as before/ deteriorated
2. Numbness or pain in the upper extremities
yes/no
during the daytime/ at night/ otherwise
no awakening/ once a week/ 2-6 times a week/ every night/ more often
change: improved/ the same as before/ deteriorated
3. Subjective hand muscle weakness
yes/no
right/ left
change: improved/ the same as before/ deteriorated
4. Pain in upper extremities
yes/no
right: fingers/ wrist/ elbow/ shoulder/ the whole upper extremity
left: fingers/ wrist/ elbow/ shoulder/ the whole upper extremity
change: improved/ the same as before/ deteriorated
5. Else
Blood pressure: right/ left extremity:
ESR Hg Urine
Cor Pulm EKG
6 The chain sawing time
(in hours)
totally
Other vibrating tools:
Appendix III
LÄÄKÄRINTUTKIMUS (Suomussalmi)
Nimi Tutkimusnumero
Anamneesi:
metsurivuodet, aiemmat leikkaukset ja sairaudet, sukusairaudet, liikunta, tupakointi,
alkoholinkäyttö, ammatti, lomautukset
Nykyoireet
Pääasiallinen ongelma (potilaan ilmoittama)
Tuki-liikuntaelimet: hoidot
lääkitykset, myös depressiolääkitys, fysikaaliset/ fysioterapeuttiset hoidot, kuntoutusjaksot
(ASLAK, tykytoiminta), muu, mikä?
Hyöty hoidoista?
STATUS
yleisstatus, vaikutelma, sydän- ja verenkiertoelimet, keuhkot, liikehdintä
Niska ja yläselkä:
inspektio, ryhti, atrofia
palpaatio (kaula- ja rintaranka, lihakset nh seudussa)
kaularangan liikkuvuus, kompressiotesti
Yläraajat:
nivelten aktiivit ja passiiviset liikeradat, AC nivel, humeroskapulaarirytmi, kipukaari
kiertäjäkalvosin testaus
TOS testaus
epikondyliittitestaus (palpaatio, provokaatiotestit)
Tinel, Phalen
Ihotunnot
Lihasvoimat
Puristusvoima/ asymmetria
Jänneheijasteet
VWF
Alaselkä:
Inspektio, ryhti
Selän liikelaajuudet, Modifioitu Schober, ekstensio, lateraaliflektiot
varvas-kantapääkävely
kyykkyyn-ylös
tasahyppely yhdellä ja kahdella jalalla
jänneheijasteet
Lasegue
lihasvoimat
ihotunnot (kosketus, kipu, vibraatio)
kaudaoire?
vatsalihasvoima (sit-up)
lonkkien rotaatiot ja trokanterbursan palpaatio
lannerangan aristus
SI niveltestit
Femoralisvenytys
ADP ja ATP palpaatio
Waddellin testit
Appendix IV
MEDICAL EXAMINATION (Suomussalmi)
Name Number
MEDICAL HISTORY:
years as a forestry worker, prior operations and diseases, heredity, sports, smoking, use of
alcohol, occupation, layoffs
Present symptoms
The main problem (by a patient)
Musculoskeletal system: therapies/ treatments
medication, also depression medication, physical/physiotherapy treatments, rehabilitation
(also in institutions), other?
Benefit from therapies/ treatments?
STATUS:
general status, general impression, heart and circulatory system, pulmonary status,
movements
Neck and upper part of trunk
inspection, posture, atrophy of muscles
palpation (cervical and thoracic spine, muscles in the neck-shoulder region)
cervical mobility, spurling
Upper extremities:
active and passive movements of joints, humeroscapular rhytm, painful arch
rotator cuff testing
TOS testing
testing of epicondylitis (palpation, provocation tests)
Tinel, Phalen
Sensory testing
Muscle strength testing
Grip force/ asymmetry
Reflexes
VWF
Lower back:
Inspection, posture
Mobility, Modified Schober, exension, lateral flexion
on tip-toe and on heels walking
Squatting
Jumping with both or one leg
Reflexes
Lasegue
Muscle testing
Sensory testing (touch, pain, vibration)
cauda equina?
stomach muscle testing (sit-up)
rotation of hip joints, palpation of trochanter bursa
tenderness of lumbar spine
SI joint palpation
Femoralis stretching
ADP ja ATP palpation
Waddell testing
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