To compare the Somatosensory Evoked Potentials
(SSEPs) and Motor Evoked Potentials (MEPs) of diabetic
and non-diabetic patients during intraoperative
monitoring of Scoliosis surgery
DISSERTATION
Module: Research Project
BMS4997
Supervisor: Dr. Marc Rayan
Date of submission: 10-09-2018
Student: MUHAMMAD ANEES SARWAR
Student ID: M00646922
M.Sc. Clinical Physiology (Neurophysiology)
MIDDLESEX UNIVERSITY
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TABLE OF ABBREVIATIONS
Abbreviation Terms
1. DM Diabetes Mellitus
2. GDM Gestational Diabetes Mellitus
3. WHO World Health Organization
4. IDF International Diabetes Federation
5. MODY Maturity-Onset Diabetes of the Young
6. CT Computed Tomography
7. MRI Medical Resonance Imaging
8. TIVA Total Intravenous Anaesthesia
9. MIS Minimally Invasive Surgery
10. EP’s Evoked Potentials
11. MEPs Motor Evoked Potentials
12. SSEPs Somatosensory Evoked Potentials
13. IONM Intraoperative Neuromonitoring
14. SCEPs Spinal Cord Evoked Potentials
15. D-Waves Direct Waves
16. EMG Electromyography
17. EEG Electroencephalography
18. SNAP Sensory Nerve Action Potentials
19. TcMEPs Transcranial Motor Evoked Potentials
20. CMAP Compound Muscle Action Potential
21. APB Abductor Pollicis Brevis
22. ADM Abductor Digiti Minimi
23. TA Tibialis Anterior
24. AH Abductor Hallucis
25. GCN Gastrocnemius
26. QUADS Quadriceps
27. amp Amplitude
28. OL Onset Latency
29. PE Pulmonary Embolism
30. DVT Deep Vein Thrombosis
31. CMCT Central Motor Conduction Time
32. PCT Peripheral Conduction Time
33. JOA Japanese Association Score
34. CCT Central Conduction Time
35. Ho Null Hypothesis
36. H? Alternative Hypothesis
37. MAC Mean Alveolar Concentration
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38. N-DM Non-Diabetic Group
39. PTN Posterior Tibial Nerve
40. MN Median Nerve
41. Fpz Prefrontal Region
42. Cz Central Region
43. ms Milliseconds
44. µV Microvolts
45. RMN Right Median Nerve
46. LMN Left Median Nerve
47. RTN Right Posterior Tibial Nerve
48. LTN Left Posterior Tibial Nerve
49. R-APB Right Abductor Pollicis Brevis
50. L-APB Left Abductor Pollicis Brevis
51. R-TA Right Tibialis Anterior
52. L-TA Left Tibialis Anterior
53. R-AH Right Abductor Hallucis
54. L-AH Left Abductor Hallucis
55. R-QUAD Right Quadriceps
56. L-QUAD Left Quadriceps
57. BAEPs Brainstem Auditory Evoked Potentials
58. VEPs Visual Evoked Potentials
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LIST OF FIGURES
Figure Page
Figure-1 Diagnosis of Diabetes Mellitus. 12
Figure-2 Complications of diabetes. 13
Figure-3 Types of scoliosis according to the spine. 14
Figure-4 Measurement of Cobb angle with an inclinometer. 17
Figure-5 Dissimilar stages of scoliosis correction surgery. 19
Figure-6 Kyphoscoliosis before and after correction surgery. 20
Figure-7 MEPs during IONM of Scoliosis correction surgery. 22
Figure-8 SSEPs and Free-run EEG within good waveform during Scoliosis
surgery.
23
Figure-9 Spinal SSEPs during Scoliosis surgery. 25
Figure-10 Lower limb muscles used for MEPs recording. 26
Figure-11 Upper limb muscles used for MEPs recording. 27
Figure-12 Free run EMG, EEG and TcMEPs during scoliosis correction
surgery.
29
Figure-13 Effect of anaesthesia on MEPs during IONM. 32
Figure-14 Corkscrew, surface electrodes and placement of corkscrew
electrodes according to the 10-20 international system.
44
Figure-15 Stimulation and recording sites of somatosensory evoked potentials. 45
Figure-16 Measurement method for amplitude and onset latency (OL). 47
Figure-17 Flowchart for analysis of the difference between interdependent
data.
48
Figure-18 Flow Chart for an analysis of the difference between independent
data.
49
Figure-19 Pie chart for percentage of gender distribution in sample size. 51
Figure-20 Bar chart for gender distribution among groups. 52
Figure-21 Bar chart representing age groups. 53
Figure-22 Bar chart illustrating age distribution according to diagnosis. 54
Figure-23 Bar chart for percentage change is SSEPs amplitude among both
groups.
77
Figure-24 Bar chart for the percentage change in SSEPs onset latency among
groups.
78
Figure-25 Bar chart for the percentage change in MEPs amplitude among
groups.
79
Figure-26 Bar chart for the percentage change in MEPs onset latency among
groups.
80
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LIST OF TABLES
Table Page
Table-1 Sample selection criteria. 41
Table-2 Non-Diabetic group median nerve SSEPs amplitude difference. 56
Table-3 Non-Diabetic group median nerve SSEPs onset latency difference. 57
Table-4 Non-Diabetic group posterior tibial nerve SSEPs amplitude
difference.
59
Table-5 Non-Diabetic group posterior tibial nerve SSEPs onset latency
difference.
60
Table-6 Diabetic group median nerve SSEPs amplitude difference. 52
Table-7 Diabetic group median nerve SSEPs onset latency difference. 63
Table-8 Diabetic group posterior tibial nerve SSEPs amplitude difference. 65
Table-9 Diabetic group posterior tibial nerve SSEPs onset latency difference. 66
Table-10 Non-Diabetic MEPs amplitude difference. 68
Table-11 Non-Diabetic MEPs onset latency difference. 70
Table-12 Diabetic group MEPs amplitude difference. 72
Table-13 Diabetic group MEPs onset latency difference. 74
Table-14 Comparison of SSEPs and MEPs among the Non-Diabetic and
Diabetic group.
76
Table-15 Median Nerve SSEPs raw data. 99
Table-16 Posterior Tibial Nerve SSEPs raw data. 100
Table-17 MEPs amplitude (µ?) raw data. 101
Table-18 MEPs onset latency (OL) raw data. 102
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TABLE OF CONTENTS
TABLE OF ABBREVIATIONS …………………………………………………………………………………. 1
LIST OF FIGURES …………………………………………………………………………………………………… 3
LIST OF TABLES …………………………………………………………………………………………………….. 4
ACKNOWLEDGEMENT ………………………………………………………………………………………….. 7
ABSTRACT ……………………………………………………………………………………………………………… 8
SECTION-I ………………………………………………………………………………………………………………. 9
INTRODUCTION:……………………………………………………………………………………………….. 10
1. Diabetes Mellitus (DM): …………………………………………………………………………………. 10
2. Scoliosis: ………………………………………………………………………………………………………. 14
3. Scoliosis Correction Surgery: ………………………………………………………………………….. 17
4. Intraoperative Neurophysiological monitoring (IONM): …………………………………….. 22
5. The rationale of the study: ………………………………………………………………………………. 33
6. Literature Review: …………………………………………………………………………………………. 33
7. The aim of the study: ……………………………………………………………………………………… 37
8. Hypothesis: …………………………………………………………………………………………………… 37
SECTION-II ……………………………………………………………………………………………………………. 38
MATERIALS AND METHODS: …………………………………………………………………………… 39
1. Study Design: ……………………………………………………………………………………………….. 39
2. Sampling Technique: ……………………………………………………………………………………… 39
3. Study Setting: ……………………………………………………………………………………………….. 39
4. Study Duration:……………………………………………………………………………………………… 40
5. Sample Size Estimation: …………………………………………………………………………………. 40
6. Sample Selection Criteria: ………………………………………………………………………………. 40
7. Ethical Consideration: ……………………………………………………………………………………. 42
8. Methodology and material used: ……………………………………………………………………… 42
9. Data Collection and Data Analysis:………………………………………………………………….. 46
SECTION-III ………………………………………………………………………………………………………….. 50
RESULTS: ………………………………………………………………………………………………………….. 51
1. Percentage of gender distribution in sample size: ………………………………………………. 51
2. The frequency of gender distribution in the groups: …………………………………………… 52
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3. Patients distribution in different age groups: ……………………………………………………… 53
4. Patients distribution in age groups according to diagnosis: …………………………………. 54
5. Question 1: Difference between baseline and closing SSEPs of Median nerve among
the non-diabetic group? ……………………………………………………………………………………… 55
6. Question 2: Difference between baseline and closing SSEPs of Posterior Tibial nerve
among the non-diabetic group? …………………………………………………………………………… 58
7. Question 3: Difference between baseline and closing SSEPs of Median nerve among
the diabetic group? …………………………………………………………………………………………….. 61
8. Question 4: Difference between baseline and closing SSEPs of Posterior Tibial nerve
among the diabetic group? ………………………………………………………………………………….. 64
9. Question 5: Difference between baseline and closing MEPs among the non-diabetic
group? ……………………………………………………………………………………………………………… 67
10. Question 6: Difference between baseline and closing MEPs among the Diabetic
group? ……………………………………………………………………………………………………………… 71
11. Question 7: Can Diabetes Mellitus lead to increase in onset latency and decrease in
amplitude during intraoperative monitoring of scoliosis correction surgery? …………….. 75
12. Percentage change in SSEPS amplitude: …………………………………………………………. 77
13. Percentage change in SSEPs onset latency: …………………………………………………….. 78
14. Percentage Change in MEPs amplitude: …………………………………………………………. 79
15. Percentage change is MEPs onset latency: ………………………………………………………. 80
SECTION-IV ………………………………………………………………………………………………………. 81
DISCUSSION: …………………………………………………………………………………………………….. 82
Limitations: …………………………………………………………………………………………………………. 89
Recommendation: …………………………………………………………………………………………………. 89
CONCLUSION: …………………………………………………………………………………………………… 90
SECTION-V …………………………………………………………………………………………………………… 91
REFERENCES: ……………………………………………………………………………………………………. 92
SECTION-VI ………………………………………………………………………………………………………….. 96
APPENDIX-I: MIDDLESEX UNIVERSITY ETHICAL FORM: ………………………………. 97
APPENDIX-II: GHURKI TRUST TEACHING HOSPITAL ETHICAL REVIEW
COMMITTEE (ERC) CERTIFICATE: …………………………………………………………………… 98
APPENDIX-III: SSEPs and MEPs raw data: ……………………………………………………………. 99
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ACKNOWLEDGEMENT
I owe an massive debt of gratitude to my supervisors, Mrs Linda Howard, Clinical
Neurophysiologist at Harley Street Clinic and Princess Grace Hospital London, and Mr
Kamran Ayoob, Clinical Neurophysiologist, Ghurki Trust Teaching Hospital Lahore Pakistan,
for their support from the formative stages of this dissertation to its final draft. Their sound
advice and careful guidance were irreplaceable. I outspread my sincere appreciation to them
for their pastoral heart, insight, patience, encouragement, positive criticism and support in
bringing this work to completion.
I also extend my gratitude and appreciation to my mentor Dr Marc Rayan, Course
Leader, M.Sc. Clinical Physiology (Neurophysiology) Middlesex University London, for the
deft ways in which he lovingly supported me throughout the whole of this work. His extreme
generosity will be remembered always.
I thankfully acknowledge the Ethical Review Committee (ERC) Ghurki Trust Teaching
Hospital, chairman Professor Amir Aziz, for their kind assistance and supervision in data
collection.
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ABSTRACT
Diabetes is a collection of metabolic syndromes categorised by the elevated level of the
glucose in the body or hyperglycemia due to the shortcoming insulin secretions from the
pancreas, defect in insulin action or both together. Scoliosis is a structural spinal deformity and
three-dimensional deviation of the spinal axis with coronal curvature beyond 10º
anteroposteriorly along with vertebral rotation and reduced kyphosis (irregular apparent shape
of the spine) in thoracic curves. Scoliosis correction surgery is used to correct the spinal
deformity. Intraoperative neurophysiological monitoring is a diagnostic method used during
brain and spinal cord surgeries to halt all possible neurological damage, to detect significant
neural structures, e.g. sensory and motor nerves during the operation and to decrease any
substantial postoperative impairment with the help of somatosensory and motor evoked
potentials. Twenty-six patients were analysed for selection criteria and allocated for diabetic
and non-diabetic groups. Amplitude and onset latency of somatosensory and motor evoked
potentials were measured from the limbs at the start of scoliosis surgery and statically
compared with the closing amplitude and onset latency for both groups to find out differences.
Wilcoxon Signed-rank and Paired T-test were used for this comparison. Variations of these
results were statically compared between diabetic and non-diabetic groups with the help of
Mann Whitney and Two-Sample T-test. P-value of the somatosensory and motor evoked
potentials amplitude and onset latency was lower than the value of alpha (? = 0.05). The
amplitude of the both somatosensory evoked potentials and motor evoked potentials were
decreased (-1.78% to -14.92%) among diabetic patients as compared to the non-diabetic
patients. Likewise, onset latency (OL) of somatosensory and motor evoked potentials was
increased among both diabetic and non-diabetic groups. But, this increase in onset latency was
significantly enlarged (0.08% to 9.79%) among people with diabetes than non-diabetic
patients. It was concluded that diabetes mellitus does affect amplitude and onset latency, but
these variations are not clinically noteworthy. These results will be helpful clinically to prevent
false alarms during spinal cord surgical procedure among diabetic patients, to facilitate the
surgical procedure precisely, and to plan the postoperative management according to the
neuromuscular status of the nerve and muscles.
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SECTION-I
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INTRODUCTION:
1. Diabetes Mellitus (DM):
Diabetes Mellitus is defined as a collection of metabolic syndromes categorised by the
elevated level of the glucose in the body or hyperglycemia due to the shortcoming insulin
secretions from the pancreas, defect in insulin action or both together. Chronic diabetes is
mostly related to the continuing damage, malfunctioning and organ failure. Diabetes frequently
affects the nerves, eyes, blood vessels, kidneys and heart in the body. Patient presents with the
sign and symptoms of weight loss, polyuria, blurred vision, polydipsia and occasionally with
the polyphagia. If diabetes remains untreated these problems convert into more severe types,
for example, peripheral neuropathy, nephropathy, retinopathy and autonomic neuropathy.
Diabetes Mellitus is mainly classified as Type-I Diabetes, Type-II diabetes and Gestational
Diabetes Mellitus (GDM) (Association, 2014). Conferring to the World Health Organization
(WHO), 108 million people were living with diabetes in 1980, which was increased four times
in 2014. The International Diabetes Federation (IDF) estimated 151 million population with
diabetes globally in 2000, which became 194 million in just three years. This number raised to
246, 285, 366, 382 and 415 million in 2006, 2009, 2011, 2013 and 2015 respectively. This data
predicts how the prevalence of diabetes has been growing over current decades. A study
assessed the prevalence of diagnosed diabetes in 2017 as 425 to 451 million depending upon
age groups. They also founded that almost 49.7% people, over 224 million adults are living
with undiagnosed diabetes (Cho et al., 2018, Khawaja et al., 2018).
1.1- Type-1 Diabetes Mellitus:
Type-I Diabetes is defined as glucose intolerance due to the insulin deficiency resulting
from the destruction of the beta cells of the pancreas. This type accounts for 5-10% of diabetes.
The known aetiology behind this type is an autoimmune pathologic process which destroys the
pancreatic beta cells and leads to the insulin deficiency. Type-1 diabetes is also known as
Juvenile diabetes because it mostly affects the young adults and children. It’s also called
insulin-dependent diabetes because patients’ needs subdermal insulin injections to maintain
glucose concentration in the blood (Association, 2014). The incidence rate of type-I diabetes
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is 40/1000000 in Finland, 1-8/1000000 in Pakistan and Egypt respectively and 0.1/1000000 in
China (Amiri et al., 2016, Patterson et al., 2014).
1.2- Type-II Diabetes Mellitus:
Type-II Diabetes is defined as glucose intolerance either due to the insulin resistance
to its action or due to insufficient insulin secretion from the pancreas eventually lead to the
hyperglycemia. This type of diabetes accounts for 90-95%. The possible aetiology behind this
type is obesity, increased percentage of the body fat and poor lifestyle. Type-II diabetes is also
known as non-insulin-dependent diabetes because drugs can increase the insulin secretion from
the pancreas or they also can decrease the insulin resistance against glucose. It’s also called
adult-onset diabetes because it mostly affects adults and old age population (Association,
2014). Prevalence of type-II diabetes in Pakistan is 11.7%. Males are more likely to get this
type of diabetes with the prevalence of 11.20% than females 9.19% (Meo et al., 2016).
1.3- Gestational Diabetes (GDM):
Gestational Diabetes Mellitus (GDM) is defined as glucose intolerance in the females
during the pregnancy which habitually disappears afterwards the birth of the child. This type
of diabetes can occur at any stage of the pregnancy but mostly recorded in the second half
(Association, 2014). A study proposed that in 2017 almost 21.3 million live births were
affected by hyperglycemia and 18.4 million cases were due to gestational diabetes mellitus
(Cho et al., 2018).
1.4- Uncommon Variants of Diabetes:
Diabetes mellitus has some other uncommon variants also. The glucose intolerance
characterizes Maturity-Onset Diabetes of the Young (MODY) due to impaired insulin
secretion without any problem with insulin action. The known cause for this variant is
monogenetic defects of the beta-cells function in the pancreas. The other pathologies which
can also lead to hyperglycemia and later diabetes include genetic defects in insulin action, e.g.
Lipoatrophic diabetes, diseases of the exocrine pancreas, e.g. Pancreatitis, endocrinopathies,
e.g. Acromegaly, Cushing syndrome, Hyperthyroidism. Drugs or chemical induced
pathologies, e.g. glucocorticoids, Thiazides, Infections, e.g. Cytomegalovirus and other
genetic syndromes, e.g. Down, Klinefelter and Turner syndrome etc. (Association, 2014).
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1.5- Diagnosis of Diabetes:
Blood glucose concentration in the blood diagnoses of diabetes. Normal fasting levels
of the blood glucose concentration are 80-100 mg/dl and normal levels after 2-3 hours taking
meal are 120-140 mg/dl. In contrast, fasting blood glucose concentration for diabetic patients
are 126+ and 2-3 hours after taking meal is 200 plus. Hb1ac is another laboratory test for
diagnosis of diabetes which measures the blood glucose concentration. Normal levels are 5%
or less than 5%, and for diabetics, this value is more than 6.5% (Gangwar et al., 2018). Patients
experience serious complications of diabetes, and these complications become more severe as
the disease progresses. A study in 2017 estimated that diabetes accounts for 9.9% of all types
of the deaths and almost 5.0 million people die each year due to diabetes (Cho et al., 2018).
Figure 1: Diagnosis of Diabetes Mellitus (Jiang, 2017).
1.7- Complications of Diabetes:
Diabetic complications are divided into macrovascular and microvascular. Diabetic
retinopathy is a microvascular complication which damages the small blood vessels to the eye
leading to visual disability or blindness. Diabetic nephropathy is another chronic microvascular
problem which affects the capillaries of the kidneys and disturbs the reabsorption, eventually
causing renal failure or even death. Diabetic neuropathy is the utmost communal microvascular
complication which arises either due to direct damage to the sensory nerves or either due to
the damage to the blood vessels supplying the nerves. This complication cause burning
sensations in hand and feet or complete sensory loss, diabetic ulcers, damage the limbs and
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may lead to amputation, cause impotence in the males, body muscles weakness and poor
wound healing. Macrovascular complications contain cardiovascular problems, e.g.
atherosclerosis. Due to hyperglycemia glucose start depositing in the walls of the large arteries
leading to the narrowing of the diameter eventually causing heart attack due to blockage of the
coronary arteries (Papatheodorou et al., 2016).
Figure 2: Complications of diabetes (Jiang, 2017).
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2. Scoliosis:
Scoliosis is a structural spinal deformity and defined as three-dimensional (3D)
deviation of the spinal axis with coronal curvature beyond 10º anteroposteriorly along with
vertebral rotation and reduced kyphosis in thoracic curves. Spine turns and curves to the side
in scoliosis. Naturally, spinal curves are present along the “sagittal plane” at the level of
cervical, thoracic and lumbar spine. These curves work as a shock absorber to dispense the
mechanical stress during the body movement and position the head over the pelvis. Scoliosis
is a deformity in “coronal or frontal plane” rather than the sagittal plane. The coronal or frontal
plane is a vertical line from the head to the foot and parallel to the shoulders. Coronal plane
divides the body into front and back sections while the sagittal plane split the body into right
and left (Trobisch et al., 2010). Scoliosis curves can be either S-shaped or C-shaped. Lumbar
and cervical curves are known as lordosis, and thoracic curves are known as kyphosis. These
curves can get worse as the child will grow. Cobb angle is used to calculate the size and angle
of the curve. Scoliosis curves with the Cobb angle more than 90º can lead to the severe
cardiopulmonary complications, with the risk of morbidity and mortality. Scoliosis is named
after the area of the spine involved, e.g. Cervical scoliosis (C1-C6), Cervicothoracic scoliosis
(C7-T1), Thoracic scoliosis (T2-T12), Thoracolumbar scoliosis (T12-L1), Lumbar scoliosis
(L2-L4) and Lumbosacral scoliosis (L5-S1) (Rolton et al., 2014).
Figure 3: Types of scoliosis according to the spine (Rolton et al., 2014).
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2.1- Non-Idiopathic Scoliosis and subtypes:
Scoliosis can be diagnosed at any age from an infant to the older adult depending upon
the pathogenesis. Generally, scoliosis is divided into non-idiopathic and idiopathic scoliosis.
Non-idiopathic scoliosis is subdivided into congenital, neuromuscular and mesenchymal
scoliosis. Congenital scoliosis is defined as spinal deformity due to embryological
malformation of the one or more vertebrae which may occur at any level (Konieczny et al.,
2012). This type of scoliosis can occur due to one of the following reasons, e.g. absence of
vertebrae, malformed vertebrae, jointed vertebrae and partially formed vertebrae. Congenital
scoliosis is not evident at the time of birth, but deformity starts as the child grow into
adolescence (Popko et al., 2018). Neuromuscular scoliosis is defined as the presence of spinal
deformity due to the insufficiency of the active stabilisers muscles to stabilise the spine
secondary to neuromuscular or neurological disorders. The most common conditions which
cause neuromuscular scoliosis includes cerebral palsy, Duchenne or Becker muscular
dystrophies, spina bifida, spinal muscle dystrophies, poliomyelitis and spinal cord injuries.
Mesenchymal scoliosis is defined as spinal deformity due to the insufficiency of the passive
stabiliser muscles to stabilise the spine. The most common problems behind this type are
Marfan’s syndrome, inflammatory diseases, mucopolysaccharidosis, open heart or thoracic
surgeries and osteogenesis imperfecta (Konieczny et al., 2012, Popko et al., 2018).
2.2- Idiopathic Scoliosis and subtypes:
Idiopathic scoliosis is defined as scoliosis without any known aetiology and accounts
for more than 90% of all scoliosis in the world. Diagnosis of the idiopathic scoliosis is made
after excluding all types of non-idiopathic scoliosis. Idiopathic scoliosis is also subdivided into
infantile, juvenile, adolescent and adult scoliosis. Infantile scoliosis is defined as the presence
of spinal deformity from the birth until the age of three (3) years without any cause. Prevalence
of this type is 1% of all types of idiopathic scoliosis. Juvenile scoliosis is defined as
development of spinal deformity at the age of 4-10 years without any known cause. Prevalence
of this type is 10-15% of idiopathic scoliosis. Adolescent scoliosis is defined as development
of spinal deformity at the age of 11-18 years without any known cause. The incidence of this
type of scoliosis is almost 90% of all types of idiopathic scoliosis. Adult scoliosis is defined as
development of the spinal deformity over the age of 18 years without any known cause.
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Prevalence of this type varies from 8%-68% depending upon the age (Trobisch et al., 2010,
Konieczny et al., 2012, Popko et al., 2018, Hresko, 2013).
2.3- Diagnosis of Scoliosis:
The patient presentation and physical examination diagnose scoliosis. Patient presents
with following signs, e.g. raised hips one or both, uneven shoulders with one shoulder edge
more protruding than the other, the head is not aligned centrally, uneven waist and ribs may be
prominent on one side. Physical examination includes “Adam’s forward bend test” in which
patient bends forward with the feet together and knees straight with arms on the side. A positive
test indicates the asymmetry in the ribs. Scoliometer is a device used to measure the angle of
the deformity known as Cobb angle, from the coronal plane in scoliosis. Further investigations
include spine, shoulder and hip x-rays, computed tomography scan (CT-scan), magnetic
resonance imaging (MRI) and laboratory tests to confirm the aetiology of scoliosis. Treatment
of scoliosis depends upon the severity of the curve. If Cobb angle is less than 25º, then
physiotherapy is advised to strengthen the active and passive stabilisers muscles. If Cobb angle
is 25º – 45º then Milwaukee brace is recommended for immature patients along with
physiotherapy plan. And if Cobb angle greater than 45º then surgical treatment is the only
option because patients may present with severe cardiopulmonary complications (Konieczny
et al., 2012, Hresko, 2013).
The Figure 4 below is illustrating the measurement method for Cobb angle with an
inclinometer. The patient is in bending position with knees straight and arms sideways reaching
toward feet. Left side is displaying a posteroanterior x-ray of a patient with kyphoscoliosis.
Thoracic spine has 26º of Cobb angle, and lumbar spine has 15º (Hresko, 2013).
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Figure 4: Measurement of Cobb angle with an inclinometer (Hresko, 2013).
3. Scoliosis Correction Surgery:
Scoliosis correction surgery is used to correct the spinal deformity. Surgery is indicated
if the Cobb angle of the growing child is more than 40º – 45º with the immature skeleton and
more than 50º in the case of adults. In the case of idiopathic scoliosis, correction surgery is
valuable to decrease the mechanical problems, e.g. chronic back pain due to spinal deformity.
This surgery is also advisable cosmetically because the patient will be more active,
independent and confident in the society. In the case of neuromuscular scoliosis, surgery is
indicated to prevent further progression of the curve, to improve wheelchair posture of the
patient, to decrease cardiopulmonary sign and symptoms and to help in nursing care. The main
objectives of the scoliosis surgery are to prevent long-term disability, to halt the progression
of the Cobb angle, to achieve good correction in frontal as well as sagittal plane and to achieve
solid fusion of the vertebrae’s (Gibson, 2004, Rolton et al., 2014).
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3.1- Posterior approach:
Scoliosis surgery team includes spine surgeon and his/her assistant, anaesthetic,
neurophysiologist, x-ray technician, operation-theatre assistant and operation-theatre nurse. A
spine surgeon is the leader of the team who decides the whole procedure. An anaesthetic doctor
prepares the patient for the surgery in the anaesthetic room by injecting intravenous anaesthetic
agents and maintain the vitals of the patients along with the anaesthesia throughout the surgical
procedure. Neurophysiologist monitors the somatosensory evoked potentials and motor
evoked potentials to prevent any possible neurological complication. Operation theatre
assistant assists the surgeon throughout the surgery in instrumentation. X-ray technician takes
the images on the demand of the surgeon during surgery. Operation theatre nurse maintains
the environment of the theatre and helps every single person in the theatre. The most common
approach used in the scoliosis is the posterior approach. When a patient is brought inside the
theatre patient is almost under a deep sleep. Patients are shifted onto the surgical table in a
prone position. Operation theatre assistant shaves and cleans the back of the patient with
povidone. Surgeon mark the Cobb angle and incision line. The incision is given along the curve
of the deformity using electrocautery. Skin and fascia are incised to reach the vertebrae. Spinal
ligaments are carved to approach the paraspinal muscles. The paraspinal muscles are reflected,
and an approach is taken to cut the interspinal ligaments. Spinal process along with the facet
joints are broken down. Harrington rod instrumentation is used in this surgery. Pedicle screws
or laminar hooks are inserted according to Cotrel-Dubousset design. Space is built between the
vertebral body and the pedicle, and the pedicle screw is embedded in the space of all targeted
vertebrae’s. The diagram below is representing the various stages during scoliosis correction
surgery including screw fixation and rod insertion. Anesthesiologist maintains Total
intravenous anaesthesia (TIVA) and gases, e.g. isoflurane, sevoflurane etc. which keeps the
patient in a deep sleep as well as preserve the blood pressure. At the end of the surgery when
pedicle screws are inserted in the all vertebrae’s, contoured rod are places to correct the
deformity in all planes. Distraction and compression are applied to provide stability. The spine
is fused by adding bone graft to the curved area of the spine. The surgeon closes the skin by
suturing the fascia and the skin. The adhesive dressing is applied on the wound to keep the
wound safe from contamination. This system allows almost 60-80% correction of the spinal
deformity as well as immediate ambulation without the need of bracing. The rate of
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neurological complications of this surgery is 0.2-1.8% (Gibson, 2004, Rolton et al., 2014,
Trobisch et al., 2010, Popko et al., 2018, Surgeons, 2018).
Figure 5: Dissimilar stages of scoliosis correction surgery. Diagram illustrating
deformed Spine, pedicle screws placement, rod placement and corrected spinal
deformity (2018).
3.2- Anterior approach:
The anterior approach is another technique in which patient lies on the side. The
surgeon makes incision anterolaterally and deflates the lung to remove the rib. The spine is
reached and fixed with screws to correct the deformity. This approach also has several
advantages, e.g. quicker rehabilitation, better curve correction, improve spine mobilisation
with fixation of fewer segments. The possible disadvantage of this approach is an elevated risk
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of morbidity and continuous need of bracing for several months. Decompressive laminectomy
is also used if the stenosis is present along with scoliosis(Surgeons, 2018). Minimally Invasive
Surgery (MIS) is a new technique with a smaller incision than posterior and anterior approach.
This technique is used in scoliosis with use of advanced fluoroscopy and endoscopy. In
juvenile and infantile scoliosis instead of Harrington rods, manually or magnetically
expandable or growing rods are used (Surgeons, 2018, Rolton et al., 2014).
The figure below is representing x-rays of a 14-year old girl with scoliosis. Left two x-
rays are demonstrating S-shaped kyphoscoliosis with 90º Cobb angle. X-rays on the right side
are depicting almost complete correction of the deformity with multiple level transpedicular
screw fixation surgery (Trobisch et al., 2010).
Figure 6: Kyphoscoliosis before and after correction surgery (Trobisch et al., 2010).
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3.3- Risks and complications:
Risk of spinal cord injury during scoliosis surgery is decreasing with the advancement
of the techniques. Scoliosis research society stated that the risk is between 0.3-0.6% and
according to another study risk of spinal cord injury is between 0.2-1.8%. The most common
cause of the neurological deficit is a contusion of the spinal cord either through tools or either
through implant itself. During surgery, radicular arteries can also get stretched or compressed
leading to the ischemic injury of the spinal cord. Sometimes, epidural hematoma and
distraction injury of the spinal cord can also cause the neurological deficit. Prolong position of
the patient on the surgical table can compress the individual nerve or blood vessel or whole
brachial plexus causing neuronal injury. Motor pathways are most commonly affected by these
types of ischemic injuries which affects anterior spinal arteries (Turner et al., 2016, Leong et
al., 2016).
The diagram below is signifying the clinical worth of intraoperative monitoring during
scoliosis surgery by comparing motor evoked potentials recorded from lower limb muscles at
various times (black line) with the baseline (green line). The symbol P is representing positive
peak and N is depicting a negative peak.
A) Motor evoked potentials after insertion of the rod into the screw for derotation. A drop
of the amplitude of more than 50% can be seen bilaterally (black line) as compared to
baseline (green line).
B) Motor evoked potentials get recovered after correction release by removal of screws
and rod.
C) The amplitude of the MEPs again declined after reinsertion of the implant.
D) Motor evoked potentials amplitude recovered again by injecting dexamethasone and
increasing mean arterial pressure (MAP) (Park and Hyun, 2015).
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Figure 7: MEPs during IONM of Scoliosis correction surgery (Park and Hyun, 2015).
4. Intraoperative Neurophysiological monitoring (IONM):
Intraoperative neurophysiological monitoring (IONM) is a method used during brain
and spinal cord surgeries to halt all possible neurological damage, to detect significant neural
structures, e.g. sensory and motor nerves during the operation and to abate any substantial
postoperative impairment (Kim et al., 2013). This modality is in use from the last three decades
to evaluate the neurological function during brain and spinal cord surgeries specifically for
scoliosis. Evidence proves that intraoperative monitoring modalities make us accessible to
critical information during operations which allow us to provide neurologically efficient results
to the patient at the end of the surgery. Intraoperative monitoring work on a principle to
stimulate either nerves or brain itself and record the response away from the site of stimulation
in the form of signals called “evoked potentials (EP’s). During scoliosis surgery IONM help
neurophysiologist to identify neurological insult and aware the surgeon to take decision
accordingly. Intraoperative neurophysiological monitoring is basically an amalgamation of
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different components including somatosensory evoked potentials (SSEPs), motor evoked
potentials (MEPs), spinal cord evoked potentials (SCEPs), direct waves (D-waves),
electromyography (EMG) and electroencephalography (EEG) (Chang et al., 2016, Mo et al.,
2017).
The figure below is representing the standard waveform with quiet similar baseline
amplitude and latencies at various times interval of lower limb somatosensory evoked
potentials (SSEPs) and free running electroencephalography (EEG) throughout the scoliosis
correction surgery. Redline is illustrating the baseline, and the green line is depicting the last
saved average. The white mark is showing that stimulation is under process. Free run EEG
waves are representing that patient under good sleep.
Figure 8: SSEPs and Free-run EEG within good waveform during Scoliosis surgery
(2018).
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4.1- Somatosensory Evoked Potentials (SSEPs):
Somatosensory Evoked Potentials (SSEPs) are defined as the repetitive stimulation of
the peripheral nerves (median/ulnar nerves for upper limb and posterior tibial/peroneal nerves
for lower limb) either mechanically or electrically and then average electrical response of the
primary sensory pathways is recorded from Fpz, Cz, C3′ and C4′ by signal averaging in the
form of action potential. This action potential is generated at the surface of the nerve so known
as sensory nerve action potential (SNAP). Somatosensory evoked potentials are used during
intraoperative neurophysiological monitoring to assess the efficiency of the sensory pathways
from the peripheral nerves. SSEPs were first used in the 1970’s but were not much popular. In
1977 Nash et al. defined the importance of the SSEPs, and they are now most common during
scoliosis surgery (Buckwalter et al., 2013). SSEPs monitors the path of the dorsal column from
the nerve to the cerebral cortex via the spinal cord. So, they can be recorded from both areas
using a corkscrew or epidural electrode respectively. Dorsal column-medial lemniscus
pathway is carried by myelinated, large diameter, fast conducting muscle and cutaneous
afferent fibres. This pathway carries a vibration, tactile discrimination, proprioception from
muscles and joints and crude or light touch. For SSEPs electrical stimulation subdermal
stimulating surface electrodes are placed on the median, ulnar or radial nerve for upper limb
and posterior tibial or peroneal nerve for lower limb. Electrical impulse excites the peripheral
nerve and generates a sensory nerve action potential which propagates towards the
contralateral sensory part of the cerebral cortex. Subdermal corkscrew active electrodes are
placed on the Cz’/ C1’/ C2’/ C3′, and C4′ and reference electrodes at Fz or Fpz as a recording
array. Nerves are usually stimulated at a frequency of 3 Hz with 0.2ms duration and an average
25mA intensity. Sensory nerve action potentials amplitude and latency are used as a
measurement criterion. SSEPs are considered abnormal if latency is increased more than 10%
or 2ms with a decrease in 50-70% amplitude. Possible mechanisms which can alter the SSEPs
amplitude and latency include ischemia, anaesthesia (volatile agents, e.g. nitrous oxide,
isoflurane), hypothermia, hypotension, mechanical compression, decreased hematocrit and
patients age, height, and length of limbs. The advantage of monitoring SSEPs is it can detect
injury suddenly even in neurologically compromised patients, and it can also record
continuously. SSEPs are also very helpful to diagnose the positional or postural injury. Studies
proved that the average sensitivity of the somatosensory evoked potentials is 92% with a range
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between 27-100%. Specificity of the SSEPs varies between 92-98%. Limitations of
somatosensory evoked potentials include the requirement of the signal averaging and it does
not monitor corticospinal pathways (Hwang et al., 2012, Park and Hyun, 2015, Azabou et al.,
2014, Gavaret et al., 2013).
The Figure 9 below depicting the standard somatosensory evoked potentials (SSEPs)
with the upright waveform from montage C3′-Fpz, Cz’-Fpz, C4′-Fpz and C5′-FPz.The
numbers P23, P13 and P35, are representing the normal positive peak latency of 23, 13 and 35
ms respectively among the average population. Likewise, N20, N11, N30 and N45 are
illustrating normal negative peak latency of 20, 11, 30 and 45 ms respectively among the
healthy population. The black line is a closing waveform, and the green line is baseline
potentials.
Figure 9: Spinal SSEPs during Scoliosis surgery (Park and Hyun, 2015).
4.2- Motor Evoked Potentials (MEPs):
Transcranial Motor Evoked Potentials (TcMEPs) or motor evoked potentials (MEPs)
are defined as monitoring the activity of the corticospinal tracts through stimulation of the
cerebral cortex at the scalp and recording the compound muscle action potential (CMAP)
directly from the muscles. This technique was first introduced in 1986. Corkscrew electrodes
are placed on the scalp C3, C4, C1, C2, Cz and 6 cm in front of the Cz according to the 10-20
international system for stimulation over the motor cortex area. Compound muscle action
potentials (CMAP) are recorded from the peripheral muscles (Hwang et al., 2012). For upper
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limb needle electrodes are placed inside one muscle from thenar eminence specifically
abductor pollicis brevis muscle (APB), abductor digiti mini (ADM) from hypothenar muscles,
1st dorsal interosseous, brachioradialis, biceps and deltoid depending upon the vertebrae
involved during scoliosis surgery. For lower limb needle electrodes are inserted into tibialis
anterior (TA), abductor halluces (AH), gastrocnemius (GCN) and quadriceps. If surgery
involves sacral nerve roots, then electrodes are also placed inside the anal sphincter and
diaphragm muscles. Diagrams below is illustrating the anatomy of some of these muscles.
Figure 10: Lower limb muscles used for MEPs recording (AMERMAN, 2018)
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Figure 11: Upper limb muscles used for MEPs recording (AMERMAN, 2018).
Stimulation intensity of the MEPs varies from 250V to 750V with duration of each
pulse 0.5 ms. The frequency of MEPs kept as 0.5 to 2 Hz because motor evoked (MEPs)
potentials do not need signal averaging. This technique of stimulation is known as train
stimulus technique. Generally, MEPs are considered abnormal based on “all or none criteria”.
Some studies suggest that MEPs should consider abnormal if the amplitude of the CMAP drops
50-80 % (Park and Hyun, 2015). According to a survey, MEPs are deemed unusual based on
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three criteria’s including threshold, amplitude and waveform during intraoperative monitoring.
Threshold level criterion states that neurological deficit can be found if more than 100V
stimulus voltage required during MEPs monitoring for more than an hour to get a response. If
this criterion is used, there will be no false positive or negative results. According to amplitude
criterion, if the amplitude of the CMAP decreases insistently during surgery when the surgeon
is placing some screw or correcting the deformity using compression or if 80% amplitude drops
as compared to the baseline, these are a truly positive sign. Waveform criteria are defined as
reformed morphology and duration of CMAP which is associated with an increase in voltage
(Langeloo et al., 2007). The advantage of using motor evoked potentials (MEPs) during
intraoperative monitoring does not require any averaging and immediate feedback is also
available. The disadvantage of monitoring MEPs includes patients’ needs bite block otherwise
lip or tongue laceration can occur. MEPs monitoring required at least partially intact motor
pathways. Another limitation is MEPs are not the modality of choice in patients with cardiac
arrhythmias, scalp burns, epilepsy and mandibular fracture (Azabou et al., 2014, Park and
Hyun, 2015, Gavaret et al., 2013).
The Figure 12 below is illustrating the Transcranial motor evoked potentials (TcMEPs),
free run electromyography (EMG) and free run electroencephalography (EEG) during
intraoperative monitoring of the scoliosis surgery. Free run EMG is running smoothly without
any spike or burst. Some interference can be seen in the right gastrocnemius (GCN) and
abductor hallucis (AH) possibly due to the surgical artefact. Transcranial MEPs can be seen
with good waveform and amplitude recorded from bilateral Abductor pollicis brevis (APB),
Quadriceps (QUADS), Tibialis Anterior (TA), Gastrocnemius (GCN) and Abductor Hallucis
(AH). The right side of the diagram is displaying stacks of MEPs recorded throughout the
scoliosis correction surgery with proper amplitude. Free running EEG is depicting the excellent
state of sleep and anaesthesia (2018).
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Figure 12: Free run EMG, EEG and TcMEPs during scoliosis correction surgery
(2018).
4.3- Spinal Motor Evoked Potentials (D-Waves):
Spinal Motor Evoked Potentials (SCMEPs) or Direct waves (D-waves) are defined as
compound action potentials generated by direct stimulation of the axons with conduction
velocity 50 m/s. Corkscrew electrodes are placed over the motor cortex for stimulation, and
compound corticospinal action potentials are recorded in the form of D-waves from the spinal
cord by inserting subdural or epidural electrodes. Stimulation is given with duration of 0.5-1
ms, intensity of 80-100 mA and frequency of 0.5-2 Hz. D-waves provided real-time feedback
and considered abnormal if amplitude drops more than 50% as compared to baseline potentials.
If D-waves show abnormal potentials during surgery, the probability of severe neurological
deficit is high after surgery, e.g. paraplegia. The advantage of D-waves is they have real
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prognostic value. They are very sensitive to changes during intramedullary spinal cord
resection tumours. Limitations of the D-waves are that they cannot be monitored in the children
and spinal levels below T12 due to less corticospinal tract fibres (Park and Hyun, 2015, Gavaret
et al., 2013).
4.4- Neurogenic Motor Evoked Potentials:
Neurogenic motor evoked potentials are also used during spinal cord surgeries. This
technique involves stimulation of the spinal cord using epidural electrodes and recording the
potentials from the peripheral nerves via surface electrodes. Electrode used for stimulation is
a flexible spinal electrode which is inserted by the surgeon proximally near the operating field
into the epidural space. Intensity is kept between 20-50 mA with a frequency of 4.1 Hz and
duration of 1ms for stimulation. Median, posterior tibial or sciatic nerve is used as recording
site (Park and Hyun, 2015, Gavaret et al., 2013).
4.5- Pedicle Screw Testing:
Pedicle screw testing is a technique which is valuable during scoliosis surgery to
evaluate the integrity of the pedicle screw with the help of triggered EMG. Normally, cortical
bone is an electrical insulator for a well-placed pedicle screw from the nerve root due to the
distance between them. But if a pedicle screw is not properly placed and breach the medial
pedicle boundary, it will irritate the nerve root which will be displayed as a CMAP. When an
incorrect screw is stimulated with the intensity of 5-30 mA, frequency of 0.8 Hz and duration
of 0.2 ms, then the myotomes of the irritated root will depict a sudden CMAP (Gavaret et al.,
2013). The advantage of this technique is it’s straightforward and highly sensitive for
transpedicular screw fixation surgeries. This technique is also useful during minimally invasive
surgeries to place the insert safely. Limitations include its less sensitive for thoracic spine
vertebrae and only provide information regarding pedicle screw integrity without any evidence
about neurological injury (Park and Hyun, 2015).
4.6- Free-running Electromyography (EMG):
Electromyography (EMG) used during intraoperative monitoring is known as free-
running electromyography or spontaneous electromyography. This type of EMG is used to
monitor specifically selected nerve root function during the spinal cord operation. EMG depicts
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real-time data from the peripheral muscles and widely used during spinal instrumentation
surgeries, e.g. scoliosis and trans pedicle screw fixation to avoid any postoperative
radiculopathy. There is no need for stimulation because its automatically runs throughout the
surgery and predict irritation to the nerve root as a waveform. Recording sites are peripheral
muscles based on their myotomes, e.g. for lower limb iliopsoas (L1), adductor longus (L2),
vastus lateralis (L3), vastus medialis (L4), tibialis anterior and extensor halluces longus (L5),
gastrocnemius and peroneus longus (S1) and perianal and urethral sphincter (S2-S5). For upper
limb supraspinatus (C4), biceps and deltoid (C5), wrist extensors (C6), wrist flexors and finger
extensors along with triceps (C7), finger flexors and hand intrinsic muscles (C8), hand intrinsic
muscles only (T1) and rectus abdominis (T6-T12). Spontaneous EMG is continued without
any baseline, any compression, surgical instrument irritation, pulling or stretching of the nerves
will display neurotonic discharges which encompass burst and spike waves (Park and Hyun,
2015, Gavaret et al., 2013).
4.7- Free-running Electroencephalography (EEG):
Electroencephalography (EEG) is also used during intraoperative neuromonitoring of
scoliosis surgery to assess the patient’s cortical functional level. This technique involves only
two channel continuous EEG to monitors the effect of the anaesthesia and sleep status during
the surgery. During deep sleep and deep anaesthesia patient’s EEG depicts a burst suppression
pattern. Correspondingly, if the level of anaesthesia gets lighter, EEG displays fast alpha
activity. Clinical neurophysiologist can share this information with the anaesthetic doctor to
maintain the anaesthetic levels (Mo et al., 2017).
4.8- Pharmacological and Physiological factors and artefacts during IONM:
Sensory and motor evoked potentials are highly sensitive to both pharmacological and
physiological factors. Inhaled anaesthetics, e.g. nitrous oxide or halogenated agent’s
isoflurane, sevoflurane can increase the latency and reduce the amplitude causing false positive
alarming criteria. While intravenous anaesthetics, e.g. propofol also have the similar effect but
to a lesser extent. Mostly intravenous agents, e.g. propofol along with ketamine or remifentanil
are used during intraoperative monitoring of scoliosis. Total intravenous anaesthesia (TIVA)
containing propofol and halogenated gases with meagre percentage are also used sometimes.
Physiological factors, e.g. hypothermia and hypotension can also decrease the amplitude and
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increase the latency (Park and Hyun, 2015). Artefacts and pitfalls can also occur during IONM
due to the surgical procedure, e.g. hammering or electrocautery. Movement of the respiratory
muscles and electrocardiography artefacts can also be noticed sometimes (Kim et al., 2013).
The figure below is illustrating the effect of anaesthesia on the motor evoked potentials.
MEPs are very sensitive and can get abolished by halogenated agents. Figure A) is representing
the drop-in amplitude due to halogenated agents in MEPs recorded from thenar muscles,
Tibialis Anterior (TA) and Abductor Hallucis (AH). Figure B) is displaying a complete loss
of MEPs due to halogenated agents but the patient had no postoperative neurological deficit
(Kim et al., 2013).
Figure 13: Effect of anaesthesia on MEPs during IONM (Kim et al., 2013).
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5. The rationale of the study:
The somatosensory and motor evoked potential baseline waveforms among diabetic
patients can be dissimilar to the non-diabetic patients. These changes can turn out to be worse
during spinal cord surgeries and affect the procedure by alerting clinical neurophysiologist as
well as the surgeon. The rationale of this study is that it can support us to comprehend the
consequence of diabetes mellitus on the peripheral nerves and spinal cord in scoliosis surgery
during intraoperative monitoring so postoperative management can be planned accordingly.
6. Literature Review:
Diabetic neuropathy is one of the foremost complications of the diabetes mellitus.
This is one of the significant microvascular problems which affects diabetic patients and causes
issues in central, peripheral and autonomic nervous systems (Khawaja et al., 2018). Diabetic
neuropathy causes ischemia of the nerve roots as well as motor pathways, e.g. corticospinal
tracts and affects the functioning motor units of the peripheral limb muscles. While recording
motor evoked potentials during intraoperative monitoring, a decrease in amplitude of
compound muscle action potentials in diabetic patients illustrates this response (Allen et al.,
2013). Diabetic neuropathy badly affects the myelin sheath of the nerve causing a decrease in
nerve impulse transmission. This effect can also be monitored by somatosensory evoked
potentials during intraoperative neuromonitoring which depicts decreased nerve conduction
velocity and increased onset latency. (Arrthy et al., 2014). The incidence of scoliosis and
diabetes together is not yet established. The possible reason for that is diabetes and scoliosis
are not very common together, but there are so many cases registered too. Diabetes can affect
the motor units firing or conduction of the nerve impulse during scoliosis correction surgeries.
SSEPs and MEPs are 106.16 times more likely to detect these neurological insults (Thirumala
et al., 2016). In chronic diabetic patients during scoliosis surgery, MEPs and SSEPs can mimic
as a false positive change and can be taken as a false alarm. These false alarms are fluctuations
in MEPs and SSEPs waveforms to a considerable level, but when the patient is awakened,
there will be no neurological problem (Galloway et al., 2010).
Nancy E. Epstein conducted a systemic review with a title “predominantly negative
impact of diabetes on spinal surgery: A review and recommendation for better preoperative
screening” in 2017. He reviewed different articles from PubMed related to the effect of
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diabetes on the spinal surgeries, e.g. possible complications, mortality, morbidity and
outcomes. He found a mortality rate of 40% among diabetic patients who underwent spinal
cord surgeries due to severe complications, e.g. myocardial infarction, pulmonary embolism
(PE) and deep vein thrombosis (DVT). He mentioned a slightly variable or negative impact of
diabetes upon cervical spine surgeries, e.g. anterior cervical fusion and posterior cervical
surgery. He said diabetic patients had significantly high genitourinary, respiratory and cardiac
complications with high rates of postoperative infections as compare to non-diabetes. He
proved statistically that diabetes has a significant impact during scoliosis correction surgeries
and can lead to high rates of mortality and morbidity. He mentioned that diabetes has an
adverse effect on the somatosensory and motor evoked potentials (SSEPs and MEPs) during
intraoperative monitoring of spinal cord surgery. He correlates JOA score after 1-year of the
operation and found that for diabetic patient’s central motor conduction times (CMCT), motor
evoked potentials (MEPs) and peripheral conduction times (PCT) were abnormal. He also
examined many other factors e.g. length of stay, epidural abscess, the rate of infection etc. and
concluded that diabetic patients have a very high frequency of perioperative complications,
morbidities, reoperation or readmission rates, longer length of stay, high rates of infections and
postoperative complications than non-diabetic patients (Epstein, 2017).
Shin JI and colleagues conducted a study to find out the effect of diabetes on scoliosis
surgery with title “Impact of glycemic control on morbidity and mortality in adult idiopathic
scoliosis patients undergoing spinal fusion” at the department of orthopaedic surgery, Icahn
School of Medicine at Mount Sinai, New York in 2017. They analysed administrative data
retrospectively. They extracted idiopathic scoliosis patients with age more than 45 years who
underwent spinal fusion between the year 2002 to 2011. They divided patients into three groups
controlled and uncontrolled diabetics along with non-diabetic groups. They compared the
postoperative complications among these groups. They concluded that controlled diabetes is a
risk factor for acute renal failure in adult patients undergoing spinal correction surgery. While
patients with uncontrolled diabetes are more likely to get postoperative deep vein thrombosis,
acute renal failure, haemorrhage, and neurological problems (Shin et al., 2017).
Nakanishi K and colleagues conducted a study with the title “electrophysiological
assessment of the motor pathway in diabetic patients with compressive cervical myelopathy”
in the department of orthopaedic surgery, Hiroshima University, Japan in 2015. They divided
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the patients into two groups. Group one was diabetic patients with compressive cervical
myelopathy and group two patients were with only compressive cervical myelopathy. They
stimulated cerebral motor cortex, and motor evoked potentials (MEPs) were recorded from
abductor digiti minimi (ADM) and abductor hallucis muscles using transcranial magnetic
stimulation. They also stimulated the ulnar and tibial nerve for somatosensory evoked
potentials (SSEPs). They compared the results using Japanese Association Score (JOA) for
cervical myelopathy. They concluded that group one JOA score was less than group two and
MEPs, peripheral conductions time (PCT) and central conduction time (CCT) was more
variable in group one as compare to group two due to diabetes (Nakanishi et al., 2015).
Hyun Mi Oh with his colleagues Young Jin Ko and Bomi Sul conducted a very similar
pilot study with the title “effects of diabetes mellitus on intraoperative monitoring of
somatosensory evoked potentials” at Seoul St. Mary’s hospital in 2015. His objective was to
find out the adverse effects of diabetes on SSEPs during intraoperative monitoring of brain
surgeries. He obtained retrospective data from a Korean urban city major hospital. He included
14 patients in his study. He allocated seven diabetic patients into one group and other seven
non-diabetic patients to another group. He excluded all possible complications which can alter
the result of the study, e.g. patients with previous spinal cord surgery, neurosurgical operations,
carpal tunnel syndrome and cerebrovascular diseases. He also excluded patients with
peripheral neuropathies. He monitored SSEPs from the median nerves during unruptured
cerebral aneurysm surgeries and craniotomies under total intravenous anaesthesia (TIVA). He
found that cortical latency (N20) was pointedly deferred symmetrically in the diabetic group
only. He also mentioned that interpeak latency (N20-P25) was increased in the diabetic group
as compared to the non-diabetic group. So, he concluded that central conduction abnormalities
could be present during intraoperative monitoring of the brain surgeries in diabetic patients
without any central lesion (Oh et al., 2015).
Arrthy S and his colleagues Vinodha R, Saravanan and Rajajeyakumar M conducted a
study with the title “evaluation of peripheral and central neuropathy in Type-2 Diabetes
Mellitus patients by using somatosensory evoked potentials” in the department of physiology,
Thanjavur Medical College, Thanjavur in 2014. He divided the patients into two groups and
allocated 40 patients in each group age within 40-60 years. Group one was a diabetic group
which includes 18 females and 22 males with diagnosed diabetes while group two was control
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group which comprises non-diabetic 18 women and 22 men. He excluded all patients with a
history of alcoholism, neuropathies, systemic diseases, renal or liver disorders and
cerebrovascular problems. He explained the testing procedure and protocol to the patients after
getting consent from them. He stimulated the median nerve bilaterally in both groups and
monitored SSEPs from sensory cortex of the brain. He concluded that SSEPs of cervical (N13)
and cortical (N20) latencies were prolonged. He also found that central conduction time (N20-
N13) was also increased. So, he summarised that type-2 diabetes mellitus affects the peripheral
as well as central somatosensory pathways in diabetic patients (Arrthy et al., 2014).
Pavol Kucera and colleagues conducted a very similar study with the title “spinal cord
lesions in diabetes mellitus. Somatosensory and motor evoked potentials and spinal conduction
time in diabetes mellitus” at the Department of Neurology, University Hospital of Comenius
University, Bratislava in 2005. They compared 20 diagnosed diabetic patients aged 35-50 years
with the control group of 30 healthy non-diabetic individuals. They stimulated the median and
fibular nerve bilaterally with intensity 20mA, duration 0.1 ms and frequency 5 Hz for
somatosensory evoked potentials (SSEPs) and recorded potentials from cerebral sensory cortex
by placing electrodes according to 10-20 international system. They measured peripheral and
central conduction time (PCT and CCT) as well as latencies. Motor evoked potentials (MEPs)
were recorded from extensor digitorum brevis and first dorsal interosseous muscle by placing
surface electrodes. They found that both peripheral and central conduction times were extended
in the diabetic group. They assumed these changes are due to a smaller number of myelinated
fibres. So, they concluded diabetes affects the myelin sheath and cause unapparent spinal cord
lesions (Kucera et al., 2005).
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7. The aim of the study:
The study aimed to inspect the effect of diabetes mellitus on intraoperative monitoring
of somatosensory evoked potentials and motor evoked potentials during scoliosis surgery.
8. Hypothesis:
The separate hypothesis was made for Amplitude (µV) and onset latency (ms).
Null hypothesis (Ho) = Diabetes Mellitus cannot lead to decrease in amplitude (µV) during
intraoperative monitoring of scoliosis correction surgery.
Alternative hypothesis (H?) = Diabetes Mellitus can lead to decrease in amplitude (µV) during
intraoperative monitoring of scoliosis correction surgery.
Null hypothesis (Ho) = Diabetes Mellitus cannot lead to increase in onset latency (ms) during
intraoperative monitoring of scoliosis correction surgery.
Alternative hypothesis (H?) = Diabetes Mellitus can lead to increase in onset latency (ms)
during intraoperative monitoring of scoliosis correction surgery.
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SECTION-II
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MATERIALS AND METHODS:
1. Study Design:
“Retrospective Cohort Study Design” was used during this study. A retrospective
cohort study or historical cohort study design is an analytical, observational longitudinal cohort
study design usually used in medical research. A cohort (group) of patients with similar
baseline characteristics and a risk factor is compared with another cohort (group) of individuals
without risk factor to determine the impact of the risk factor on the incidence of the condition
such as disease. These studies are carried out in present time, but data was taken from the past
events and reconstructed to examine the medical outcomes. In this study cohort of the patients
who underwent scoliosis correction surgery with a risk factor for diabetes mellitus were
compared with the group of the individuals who experienced scoliosis correction surgery
without diabetes mellitus. The advantage of using this study design is we can calculate the rate
of disease over time, can collect the data about a sequence of events and its virtuous for
inspecting unfamiliar experience. The disadvantage is we have less control over variables and
to some extent, this design is susceptible to information or recalls bias (Song and Chung, 2010,
Lwanga et al., 1991).
2. Sampling Technique:
“Non-probability Convenience Sampling Technique” was used to gather a sample for
this study. Non-probability convenience sampling technique is the opposite to the probability
sampling. We do not calculate the odds of the members being selected for a sample and sample
data is collected somewhere convenient to the researcher. The advantage of this sampling
technique is its very time and cost effective as well as easy to use, and disadvantage is it’s
almost impossible to represent the population well.
3. Study Setting:
This study was conducted at the “Orthopaedic & Spine Centre Ghurki Trust Teaching
Hospital Lahore, Pakistan”. Ethical consent was granted from the ethical committee of the
Ghurki Trust Teaching Hospital before the commencement of this study. The ethical approval
letter is attached in the appendix.
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4. Study Duration:
The total time frame for this study was three months including six weeks of data
collection.
5. Sample Size Estimation:
The sample size was premeditated by using the World Health Organization (WHO)
software. The sample size (n) calculated was twenty-six (26). The formula used for estimation
of sample size is given below (Kasiulevi?ius et al., 2006, Song and Chung, 2010).
(Sample Size determination in health studies version 2.0.21 WHO (Lwanga et al., 1991).
6. Sample Selection Criteria:
Sample selection criteria were made before the commencement of this study. Patients
were allocated into two groups including Diabetic group and Non-Diabetic group. Inclusion
and exclusion criteria were defined. Patients with age between three (3) years to thirty (30)
years were included in the study and patients below age three (3) years and above thirty (30)
years were excluded from the study. The reason was that under age three (3) the somatosensory
and motor evoked potentials pathways are not adequately developed and patients above age
thirty (30) years are more likely to be present with comorbidities which can affect the
somatosensory and motor evoked potentials. Both male and female patients were contained
within in the study. Types of scoliosis were defined, and patients with idiopathic scoliosis and
congenital scoliosis were included in the study. All patients with neuromuscular scoliosis were
excluded from the study because in neuromuscular scoliosis both somatosensory and motor
evoked potentials are already compromised which can cause false positive results. Types of
the diabetes mellitus were also evaluated for sample selection criteria. Patients with Type-I
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and Type-II diabetes mellitus were included in the study and patients with gestational diabetes
were excluded from the study.
Total Intravenous Anesthesia (TIVA) and halogenated agents along with analgesics
were included as anaesthesia during the surgery in the study because they are usually used
during scoliosis correction surgery to allow intraoperative monitoring to detect any possible
injury. Propofol and Remifentanil in TIVA and Isoflurane, Sevoflurane and Desflurane etc. as
an inhalational agent were used with mean alveolar concentration (MAC) less than 0.5.
Inhalational agents with MAC value more than 0.5 can alter the somatosensory and motor
evoked potentials. Neuromuscular blocking agents, e.g. Pancuronium, Rocuronium,
Atracurium etc. were treated as exclusion criteria because they can cause blockage of nerve
impulse transmission at the neuromuscular junction leading to complete blockage of motor
evoked potentials. Patients with all diverse types of scoliosis curvatures were included in the
study, for example, Kyphoscoliosis and lumbosacral scoliosis. Patients with any comorbidities,
e.g. peripheral neuropathies, neuromuscular disorders, myopathies etc. which can disturb the
amplitude and onset latency of somatosensory and motor evoked potentials were excluded
from the study. Each patient history and data was strictly assessed for the inclusion and
exclusion criteria before including in the study.
Table 1: Sample selection criteria.
Inclusion Criteria
Exclusion Criteria
Age Age between 3 to 30 years Above 30 years and below
three years
Gender Both male and female
nil
Scoliosis Idiopathic and congenital
scoliosis
Neuromuscular Scoliosis
Diabetes Type-1 and Type-2 diabetes
Gestational diabetes
Anaesthesia Propofol (TIVA), Analgesics
and Halogenated agents, e.g.
Sevoflurane with MAC < 0.5
Neuromuscular blockers
Curvature Kyphoscoliosis, lumbar
scoliosis
nil
Comorbidities nil Peripheral neuropathies and
myopathies
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7. Ethical Consideration:
Ethical consent was granted from the “Ethical review committee” (ERC) of the Ghurki
Trust Teaching Hospital as well as from Middlesex University. Both letters are attached in the
appendix section. Patients personal information was not needed or used at any time during this
study.
8. Methodology and material used:
Last five (5) years somatosensory and motor evoked potentials (SSEPs & MEPs) data
in the form of amplitude and onset latency were collected from the Neurophysiology
department of the Orthopedic & Spine Centre Ghurki Trust Teaching Hospital Lahore,
Pakistan. Twenty-six (26) patients were included in the study. Two groups were made, thirteen
(13) patients who underwent scoliosis correction surgery with diabetes were allocated into a
Diabetic group (DM group). Thirteen (13) patients who experienced scoliosis correction
surgery and were non-diabetic, were included into a Non-Diabetic group (N-DM group). Each
patient was assessed for sample selection criteria.
The patient was prepared for the scoliosis correction surgery and taken into an
anaesthetic room. Propofol was injected intravenously for deep sleep, and remifentanil was
used to suppress the surgical pain. Electrodes are placed inside the anaesthetic room. A bite
blocker was inserted in the mouth to avoid any injury to the tongue, and the patient was
positioned prone on the surgical table. Somatosensory evoked potentials (SSEPs) were
recorded by stimulating bilateral median nerve (MNº) in upper limb and bilateral posterior
tibial nerve (PTNº) in the lower leg. Surface electrodes were placed at the frontal surface of
the wrist just proximal to the carpal tunnel for median nerve somatosensory evoked potentials.
Similarly, surface electrodes were placed behind the medial malleolus of the tibia bone
just near the foot where the posterior tibial nerve is superficial to stimulate the nerve for
somatosensory evoked potentials. Somatosensory evoked potentials were recorded from the
sensory cortex of the brain by inserting corkscrew electrodes in the scalp at prefrontal region
(Fpz), the central region (Cz) and sensory area 3-4 cm lateral to the central region (C3 & C4).
The stimulation parameters were within the frequency of 3 to 5 Hz with 0.2 to 300 ms duration
and intensity of 20 mA for upper limb and 30 mA for lower limb. Median and posterior tibial
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nerves were stimulated, and somatosensory evoked potentials were recorded in the form of
somatosensory nerve action potentials (SNAPs) as a baseline recording before the
commencement of the surgery.
The figure 14 below is displaying distinct types of electrodes which we used during
intraoperative monitoring of the scoliosis correction surgery. The blue electrode is a corkscrew
electrode which was used at the cortical region for stimulation of motor evoked potentials and
recording of somatosensory evoked potentials. Electrode with yellow and black wires is a
needle electrode which is inserted into the muscles and was used for recording of compound
muscle action potential (CMAP) from the muscles. The depiction in the middle is a surface
electrode which was used for stimulation of median and posterior tibial nerves. And the last
photograph is depicting the placement of the corkscrew electrodes according to the 10-20
international system for somatosensory evoked potentials recording site, and motor evoked
potentials stimulating site.
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Figure 14: Corkscrew, surface electrodes, needle electrodes and placement of corkscrew
electrodes according to 10-20 international system.
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The figure 15-A below is depicting the stimulation site (median nerve) and recording
sites (Fz-C3′), Cervical (C5) and Erb’s (EP) for upper limb somatosensory evoked potentials
(SSEPs). Similarly, figure 15-B is illustrating the stimulation site (posterior tibial nerve) at
popliteal fossa and recording site (Fz-C4′), Thoracic (T6 ; 12) and Lumbar (L3) for lower
limb somatosensory evoked potentials.
Figure 15: Stimulation and recording sites of somatosensory evoked potentials (Singh,
2016).
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Motor Evoked potentials (MEPs) were recorded from the four muscle groups
bilaterally. Needle electrodes were placed inside abductor pollicis brevis (APB) for upper limb
and tibialis posterior (TA), abductor hallucis (AH) and quadriceps (QUAD) for lower limb
muscles. Corkscrew electrodes were placed inside the scalp above the motor cortex for
stimulation. Stimulation intensity of the MEPs varies from 250V to 750V with duration of each
pulse between 0.5 to 3 ms and inter-stimulus interval of 1-5 ms. The frequency of MEPs was
kept as 0.5 to 2 Hz because there was no need for averaging for muscle MEPs. Motor cortex
was stimulated to record the compound muscle action potentials (CMAP) from the all muscle
groups as a baseline. When surgery was commenced, free run electromyography (EMG) was
used to detect any potential injury to the nerve root in the form of burst or spike. Two channel
free run electroencephalography (EEG) was used to keep an eye on the sleep status of the
patient.
Both sensory nerves and motor cortex were stimulated throughout the surgery at
different intervals to record somatosensory and motor evoked potentials waveform to avoid
any potential harm to the patients. Both remifentanil and propofol were maintained as trans
intravenous anaesthesia (TIVA). Patient temperature, blood pressure, heart rate and pulse were
recorded after every 15 minutes interval to correlate any change in the SSEPs or MEPs
waveforms. After completion of the operation, closing MEPs and SSEPs were recorded. All
twenty-six (26) cases underwent the same surgical procedure of scoliosis correction surgery
with the same conditions.
9. Data Collection and Data Analysis:
Amplitude in microvolts (µV) and onset latency in milliseconds (ms) was measured
from baseline as well as from closing waveforms of both somatosensory and motor evoked
potentials. Amplitude (figure-16) is a peak to peak value between the positive peak and
negative peak of the action potential which represents the number of the conducting fibres.
Onset latency (figure-16) is a measurement of the conductivity time of the fastest fibres from
the stimulation site to the recording electrodes. Data was presented in the form of tables for
both Diabetic (DM) and Non-Diabetic (N-DM) groups. Data of median and posterior tibial
nerve SSEPs and muscle MEPs is given in the appendix in tabulated form. The figure below
is representing how to measure onset latency (OL) and amplitude (amp).
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Figure 16: Measurement method for amplitude and onset latency (OL).
After completion of data collection, data were analysed by using Minitab 17 statistical
software to test the hypothesis. The null hypothesis of the study was that diabetes mellitus
could not lead to increase in onset latency and decrease in amplitude during intraoperative
monitoring of scoliosis correction surgery. And alternative hypothesis (H?) was that Diabetes
Mellitus could lead to increase in onset latency and decrease in amplitude during intraoperative
monitoring of scoliosis correction surgery. To test this hypothesis, new questions were
established and analysed by creating a new hypothesis. Based on the results of the new
hypothesis central hypothesis was tested in the end. To find out the difference in baseline
amplitude and onset latency from the closing amplitude and onset latency a hypothesis was
made to compare baseline amplitude with closing amplitude and baseline onset latency with a
closing onset latency of the median and posterior tibial nerves of the diabetic group as well as
for the non-diabetic group. Null hypothesis (Ho) was there is no difference between baseline
and closing amplitude while the alternative hypothesis (H?) was there is the difference between
the baseline and the closing amplitude of SSEPs. A similar hypothesis was made for onset
latency also in which null hypothesis (Ho) was there is no difference between baseline and
closing onset latency while alternative hypothesis (H?) was there is the difference between
baseline and closing onset latency of SSEPs. Data were analysed for the differences by plotting
boxplot to get the mean values. Because data was not time series and consisted of two groups
with dependent samples between the groups, normal distribution was confirmed. A
significance level of 0.05 was defined and a paired T-test was applied for normally distributed
data, and Wilcoxon Signed Rank test was administered on ranked differences of data which
was not normally distributed. P-value was used to define the results if P ? (0.05) then
we believed on null hypothesis (Ho) which was there is no difference.
Correspondingly, to find out differences in baseline amplitude and onset latency from
closing amplitude and onset latency of motor evoked potentials (MEPs) a hypothesis was made
for all muscle group. Null hypothesis (Ho) was there is no difference in baseline and closing
amplitude and the alternative hypothesis (H?) was there is the difference between the baseline
and closing amplitude of MEPs. Likewise, for onset latency null hypothesis (Ho) was there is
no difference between baseline and closing onset latency and the alternative hypothesis (H?)
was there is the difference between baseline and closing onset latency of MEPs. Data were
analyzed for the differences by plottingng boxplot to get the mean values. Because data was
not time series and consisted of two groups with dependent samples between the groups,
normal distribution was confirmed. A significance level of 0.05 was defined, and a paired T-
test was applied for normally distributed data, and Wilcoxon Signed Rank test was applied on
ranked differences of data which was not normally distributed. P-value was used to define the
results if P ? (0.05) then we believed on null hypothesis (Ho) which was there is no
difference.
Figure 17: Flowchart for analysis of the difference between interdependent data.
Analysis of
Difference Yes
Have
Means Yes
Time Series
data No Two Groups
Yes Samples are
dependent in the
groups
Yes
Normal
Distribution
Yes
Paired T-test
? = 0.05
NO
Wilcoxon Signed Rank
Test
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The main hypothesis was analyzed by comparing diabetic baseline amplitude and onset
latency with the non-diabetic baseline amplitude. Likewise, closing amplitude and onset
latency of the diabetic group was compared with the closing amplitude and onset latency of
the non-diabetic group both for somatosensory and motor evoked potentials. The hypothesis
was tested for the difference by plotting boxplot to get the mean values. Data was not time
series and was consisted of two groups with samples independent between the groups. Normal
distribution and equal variance were confirmed. Two-Sample T-test was applied on data with
equal variance and normal distribution, and Mann Whitney test was administered on data with
unequal variance and not normally distributed. A significance level of 0.05 was defined. P-
value was used to determine the results if P ? (0.05) then we believed on null hypothesis (Ho) which was that Diabetes
Mellitus could not lead to significant increase in onset latency and a significant decrease in
amplitude during intraoperative monitoring of scoliosis correction surgery.
Figure 18: Flow Chart for an analysis of the difference between independent data.
Analysis of
Difference Yes
Have
Means Yes
Time Series
data No Two Groups
Yes Samples are
dependent in the
groups
No
Normal
Distribution and
Equal Variance
Yes
Two Sample T-test
NO
Mann Whitney
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SECTION-III
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RESULTS:
1. Percentage of gender distribution in sample size:
26 patients were enrolled in the study which was consisted of 15 (58%) females and 11
(42%) males. The percentage of male to female is given below in the form of the pie chart.
Figure 19: Pie chart for percentage of gender distribution in sample size.
Female
58%
Male
42%
Percentage of Male and Female
Female
Male
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2. The frequency of gender distribution in the groups:
Out of 26 patients, 13 patients were enrolled in the diabetic group, and 13 patients were
allocated in the non-diabetic group. The diabetic group consisted of 6 males and seven females
while the non-diabetic group consisted of 5 males and eight females. The bar chart below is
depicting this gender distribution below.
Figure 20: Bar chart for gender distribution among groups.
6
5
7
8
0
1
2
3
4
5
6
7
8
9
DiabeticNon-Diabetic
Gender distribution among groups
MaleFemale
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3. Patients distribution in different age groups:
Inclusion criteria for the age were 03 years to 30 years. All 26 patients were distributed
among different age groups. The mean age calculated was 16.19 with a standard deviation of
6.91. The range of the age was minimum six years and maximum 28 years. Four (4) patients
were between 03-07 years, five (5) patients were between 08-12 years, and five (5) patients
were between 13-17 years. Age group 18-22 years and 23-30 years consisted of six (6) patients
in each group. The bar chart below is displaying this age distribution among different age
groups.
Figure 21: Bar chart is representing age groups.
4
55
66
0
1
2
3
4
5
6
7
Frequency
Age Groups
03-07 years08-12 years13-17 years18-22 years23-30 years
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4. Patients distribution in age groups according to diagnosis:
Patients were distributed among groups using non-probability convenience sampling.
Group 03-07 years had one diabetic and three non-diabetic patients. Group 08-12 had three ;
two; group 13-17 had two and three, group 18-22 years had three in each and group 23-30
years had four diabetic and two non-diabetic respectively.
Figure 22: Bar chart illustrating age distribution according to diagnosis.
1
3
2
3
4
3
2
33
2
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
03-07 years08-12 years13-17 years18-22 years23-30 years
Age distribution according to diagnosis
DiabeticNon-Diabetic
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5. Question 1: Difference between baseline and closing SSEPs of Median
nerve among the non-diabetic group?
P-value was used to define the results when P ? (0.05) we believed on null
hypothesis (Ho) which was there is no difference.
5.1- Non-diabetic group median nerve SSEPs amplitude (amp):
Null hypothesis (Ho) = There is no difference between baseline and closing amplitude of
median nerve among the non-diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing amplitude
of median nerve among the non-diabetic group.
Baseline amplitude of the median nerve was compared with the closing amplitude of
the median nerve of the same group. The table below is demonstrating that a paired T-test was
used for both rights and left median nerve (RMN ; LMN) SSEPs. Paired T-test was used
because we were analyzing difference with data which was not time series but had means, two
groups, interdependent samples and normal distribution. For the right median nerve channel
one (Fpz-C3) we accepted the null hypothesis because of P ; ? (0.05). For right median nerve
channel two and left median nerve both channels we rejected the null hypothesis and accepted
alternative hypothesis because of P ; ? (0.05).
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Table 2: Non-Diabetic group Right and left median nerve (RMN ; LMN) SSEPs
amplitude difference:
Median Nerve SSEPs Amplitude (µ?) Difference Baseline Vs Closing
Non-Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Fpz-C3)
RMN Baseline
4.469
0.772
0.068
Paired T-
Test
T= -1.90
P – Value
0.082
3.11% P ; ? = Ho
RMN Closing
4.608 0.710 0.110
Channel 2:
(C3-C4)
RMN Baseline
4.092
0.755
0.621
Paired T-
test
T= -4.39
P – Value
0.001
5.08 % P ; ? = H1
RMN Closing
(C3-C4)
4.300 0.805 0.398
Channel 1:
(Fpz-C3)
LMN Baseline
4.285
0.894
0.143
Paired T-
test
T= – 2.29
P – Value
0.041
3.22% P ; ? = H1
LMN Closing
(Fpz-C3)
4.423 0.901 0.230
Channel 2:
(C3-C4)
LMN Baseline
3.908
1.124
0.471 Paired T-
test
T= – 4.76
P – Value
0.000
5.70% P ? (0.05).
Table 3: Non-Diabetic right and left group median nerve (RMN ; LMN) SSEPs onset
latency difference:
Median Nerve SSEPs Onset Latency (ms) Difference Baseline Vs Closing
Non-Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Fpz-C3)
RMN Baseline
15.838
2.372
0.635
Paired T-
Test
T= -2.16
P – Value
0.051
0.93% P ; ? = Ho
RMN Closing 15.985 2.509 0.691
Channel 2:
(C3-C4)
RMN Baseline
15.346
1.909 0.471
Paired T-
test
T= -1.02
P – Value
0.329
0.55 % P ; ? = Ho
RMN Closing 15.431 2.039 0.510
Channel 1:
(Fpz-C3)
LMN Baseline
14.60
1.892
0.399
Paired T-
test
T= – 2.76
P – Value
0.017
1.21% P ; ? = Ho
LMN Closing 14.785 2.037 0.352
Channel 2:
(C3-C4)
LMN Baseline
14.462
2.422 0.814
Paired T-
test
T= – 2.40
P – Value
0.034
1.49% P ; ? = Ho
LMN Closing 14.677 2.385 0.876
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6. Question 2: Difference between baseline and closing SSEPs of Posterior
Tibial nerve among the non-diabetic group?
P-value was used to define the results when P ? (0.05) we believed on null
hypothesis (Ho) which was there is no difference.
6.1- Non- diabetic group posterior tibial nerve SSEPs amplitude (amp):
Null hypothesis (Ho) = There is no difference between baseline and closing amplitude of
posterior tibial nerve among the non-diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing amplitude
of posterior tibial nerve among the non-diabetic group.
Baseline amplitude of the posterior tibial nerve was compared with the closing
amplitude of the posterior tibial nerve of the same group. The table below is elaborating that
Wilcoxon Signed Rank test was applied for channel one (Cz-Fpz) of both rights and left tibial
nerve (RTN ; LTN) because we were analyzing difference for the data which was not time
series but have means, two groups, interdependent samples and non-normal distributed. Paired
T-test was applied for channel two (C4-C3) of both rights and left tibial nerve (RTN ; LTN)
because we were analyzing difference with data which was not time series but had means, two
groups, interdependent samples and normal distribution. For both channels of right median
nerve as well as left median nerve we accepted the null hypothesis because of P ; ? (0.05).
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Table 4: Non-Diabetic group right and left posterior tibial nerve (RTN ; LTN) SSEPs
amplitude difference:
Posterior Tibial Nerve SSEPs Amplitude (µ?) Difference Baseline Vs Closing
Non-Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In
Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Cz-Fpz)
RTN Baseline
4.454
0.732
0.034
Wilcoxon
Signed
Rank
M= -0.05
P – Value
0.374
0.67% P ; ? = Ho
RTN Closing 4.485 0.719 0.018
Channel 2:
(C4-C3)
RTN Baseline
4.185
0.689
0.229
Paired T-
test
T= -0.69
P – Value
0.502
0.72 % P ; ? = Ho
RTN Closing 4.215 0.746 0.089
Channel 1:
(Cz-Fpz)
LTN Baseline
4.246
1.094
0.007
Wilcoxon
Signed
Rank
M= 0.00
P – Value
0.592
0.54% P ; ? = Ho
LTN Closing 4.269 0.863 0.012
Channel 2:
(C4-C3)
LTN Baseline
4.031
0.857
0.448 Paired T-
test
T= – 1.43
P – Value
0.180
1.51% P ; ? = Ho
LTN Closing 4.092 0.877 0.194
6.2- Non-diabetic group posterior tibial nerve SSEPs onset latency (OL):
Null hypothesis (Ho) = There is no difference between baseline and closing onset latency of
the posterior tibial nerve among the non-diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing onset
latency of the posterior tibial nerve among the non-diabetic group.
Baseline onset latency of the posterior tibial nerve was compared with the closing onset
latency of the posterior tibial nerve of the same group. The table below is signifying that the
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paired T-test was used for both channels of the right posterior tibial nerve (RTN) SSEPs. Paired
T-test was used because we were analyzing difference with data which was not time series but
had means, two groups, interdependent samples and normal distribution. And Wilcoxon
Signed Rank test was applied for both channels of left tibial nerve (LTN) because we were
analyzing difference for the data which was not time series but have means, two groups,
interdependent samples and non-normal distributed. For both channels of right median nerve
as well as left median nerve we accepted the null hypothesis because of P ; ? (0.05).
Table 5: Non-Diabetic group right and left posterior tibial nerve (RTN ; LTN) SSEPs
onset latency difference:
Posterior Tibial Nerve SSEPs Onset Latency (ms) Difference Baseline Vs Closing
Non-Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Cz-Fpz)
RTN Baseline
25.78 4.371
0.059
Paired T-
Test
T= -0.51
P – Value
0.621
0.12% P ; ? = Ho
RTN Closing 25.81 4.305 0.105
Channel 2:
(C4-C3)
RTN Baseline
25.37
4.332
0.098
Paired T-
test
T= -0.72
P – Value
0.487
0.12 % P ; ? = Ho
RTN Closing 25.40 4.245 0.090
Channel 1:
(Cz-Fpz)
LTN Baseline
24.90
4.796
0.045
Wilcoxon
Signed
Rank
M= -0.05
P – Value
0.625
0.12% P ; ? = Ho
LTN Closing 24.93 4.868 0.05
Channel 2:
(C4-C3)
LTN Baseline
25.16
4.680
0.005
Wilcoxon
Signed
Rank
M= 0.05
P – Value
0.683
-0.04% P ; ? = Ho
LTN Closing 25.15 4.616 0.077
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7. Question 3: Difference between baseline and closing SSEPs of Median
nerve among the diabetic group?
P-value was used to define the results when P ? (0.05) we believed on null
hypothesis (Ho) which was there is no difference.
7.1- Diabetic group median nerve SSEPs amplitude (amp):
Null hypothesis (Ho) = There is no difference between baseline and closing amplitude of
median nerve among the diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing amplitude
of median nerve among the diabetic group.
Baseline amplitude of the median nerve was compared with the closing amplitude of
the median nerve of the same group. The table below is demonstrating that a paired T-test was
used for both rights and left median nerve (RMN ; LMN) SSEPs. Paired T-test was used
because we were analyzing difference with data which was not time series but had means, two
groups, interdependent samples and normal distribution. For both channels of right and left
median nerve we rejected the null hypothesis and accepted alternative hypothesis because of
P ; ? (0.05).
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Table 6: Diabetic group right and left median nerve (RMN ; LMN) SSEPs amplitude
difference:
Median Nerve SSEPs Amplitude (µ?) Difference Baseline Vs Closing
Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Fpz-C3)
RMN Baseline
2.738 0.837 0.848 Paired T-
test
T= 4.11
P – Value
0.001
-11.79% P ; ? = H1
RMN Closing 2.415 0.838 0.765
Channel 2:
(C3-C4)
RMN Baseline
2.762 0.781 0.895 Paired T-
test
T= 5.51
P – Value
0.000
-13.11% P ; ? = H1
RMN Closing 2.400 0.825 0.301
Channel 1:
(Fpz-C3)
LMN Baseline
2.846 1.162 0.461 Paired T-
test
T= 4.20
P – Value
0.001
-14.87% P ; ? = H1
LMN Closing 2.423 0.985 0.955
Channel 2:
(C3-C4)
LMN Baseline
2.777 1.061 0.793 Paired T-
test
T= 6.20
P – Value
0.000
-13.03% P ; ? = H1
LMN Closing 2.415 1.002 0.353
7.2- Diabetic group median nerve SSEPs onset latency (OL):
Null hypothesis (Ho) = There is no difference between baseline and closing onset latency of
the median nerve among the diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing onset
latency of the median nerve among the diabetic group.
Baseline onset latency of the median nerve was compared with the closing onset latency
of the median nerve of the same group. The table below is demonstrating that a paired T-test
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was used for both rights and left median nerve (RMN ; LMN) SSEPs. Paired T-test was used
because we were analyzing difference with data which was not time series but had means, two
groups, interdependent samples and normal distribution. For both channels of right and left
median nerve we rejected the null hypothesis and accepted alternative hypothesis because of
P ; ? (0.05).
Table 7: Diabetic group right and left median nerve (RMN ; LMN) SSEPs onset latency
difference:
Median Nerve SSEPs Onset Latency (ms) Difference Baseline Vs Closing
Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value
of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Fpz-C3)
RMN
Baseline
15.308 2.018 0.609 Paired T-
test
T= -4.36
P – Value
0.001
7.04% P ; ? = H1
RMN Closing 16.385 2.688 0.177
Channel 2:
(C3-C4)
RMN
Baseline
15.000 2.256 0.668 Paired T-
test
T= -5.35
P – Value
0.000
8.00% P ; ? = H1
RMN Closing 16.200 2.769 0.878
Channel 1:
(Fpz-C3)
LMN
Baseline
15.177 2.146
0.679 Paired T-
test
T= -4.56
P – Value
0.001
9.43% P ; ? = H1
LMN Closing 16.608 2.885 0.755
Channel 2:
(C3-C4)
LMN
Baseline
15.092 2.390 0.717 Paired T-
test
T= -4.62
P – Value
0.001
10.14% P ; ? = H1
LMN Closing 16.623 3.346 0.146
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8. Question 4: Difference between baseline and closing SSEPs of Posterior
Tibial nerve among the diabetic group?
P-value was used to define the results when P ? (0.05) we believed on null
hypothesis (Ho) which was there is no difference.
8.1- Diabetic group posterior tibial nerve SSEPs amplitude (amp):
Null hypothesis (Ho) = There is no difference between baseline and closing amplitude of
posterior tibial nerve among the diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing amplitude
of posterior tibial nerve among the diabetic group.
Baseline amplitude of the posterior tibial nerve was compared with the closing
amplitude of the posterior tibial nerve of the same group. The table below is demonstrating
that a paired T-test was used for both rights and left posterior tibial nerve (RTN ; LTN) SSEPs.
Paired T-test was used because we were analyzing difference with data which was not time
series but had means, two groups, interdependent samples and normal distribution. For both
channels of right and left median nerve we rejected the null hypothesis and accepted alternative
hypothesis because of P ; ? (0.05).
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Table 8: Diabetic group right and left posterior tibial nerve (RTN ; LTN) SSEPs
amplitude difference:
Posterior Tibial Nerve SSEPs Amplitude (µ?) Difference Baseline Vs Closing
Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Cz-Fpz)
RTN Baseline
2.938 0.856 0.238 Paired T-
test
T= 5.38
P – Value
0.000
-15.18% P ; ? = H1
RTN Closing 2.492 0.786 0.306
Channel 2:
(C4-C3)
RTN Baseline
2.885 0.815 0.138 Paired T-
test
T= 5.90
P – Value
0.000
-14.66% P ; ? = H1
RTN Closing 2.462 0.699 0.058
Channel 1:
(Cz-Fpz)
LTN Baseline
3.362 1.094 0.235 Paired T-
test
T= 7.10
P – Value
0.000
-14.19% P ; ? = H1
LTN Closing 2.885 1.078 0.118
Channel 2:
(C4-C3)
LTN Baseline
2.969 1.061 0.708 Paired T-
test
T= 5.25
P – Value
0.000
-13.98% P ; ? = H1
LTN Closing 2.554 0.935 0.757
8.2- Diabetic group posterior tibial nerve SSEPs onset latency (OL):
Null hypothesis (Ho) = There is no difference between baseline and closing onset latency of
the posterior tibial nerve among the diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing onset
latency of the posterior tibial nerve among the diabetic group.
Baseline onset latency of the posterior tibial nerve was compared with the closing onset
latency of the posterior tibial nerve of the same group. The table below is elaborating that
Wilcoxon Signed Rank test was applied for both channels of right and left tibial nerve (RTN
; LTN) because we were analyzing difference for the data which was not time series but have
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means, two groups, interdependent samples and non-normal distributed. For both channels of
right and left median nerve we rejected the null hypothesis and accepted alternative hypothesis
because of P ; ? (0.05).
Table 9: Diabetic group right and left posterior tibial nerve (RTN ; LTN) SSEPs onset
latency difference:
Posterior Tibial Nerve SSEPs Onset Latency (ms) Difference Baseline Vs Closing
Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
Channel 1:
(Cz-Fpz)
RTN Baseline
27.48 3.536 0.018
Wilcoxon
Signed Rank
M= -0.70
P – Value
0.002
2.98% P ; ? = H1
RTN Closing 28.3 3.309 0.034
Channel 2:
(C4-C3)
RTN Baseline
28.18 2.558 0.017 Wilcoxon
Signed Rank
M= -0.65
P – Value
0.002
2.45% P ; ? = H1
RTN Closing 28.87 2.629 0.009
Channel 1:
(Cz-Fpz)
LTN Baseline
27.72 3.088 0.005 Wilcoxon
Signed Rank
M= -0.65
P – Value
0.002
2.31% P ; ? = H1
LTN Closing 28.36 3.133 0.005
Channel 2:
(C4-C3)
LTN Baseline
28.08 2.749 0.072 Wilcoxon
Signed Rank
M= -0.65
P – Value
0.002
2.28% P ; ? = H1
LTN Closing 28.72 2.787 0.005
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9. Question 5: Difference between baseline and closing MEPs among the
non-diabetic group?
P-value was used to define the results when P ? (0.05) we believed on null
hypothesis (Ho) which was there is no difference.
9.1- Non-diabetic group MEPs amplitude (amp):
Null hypothesis (Ho) = There is no difference between baseline and closing amplitude of MEPs
among the non-diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing amplitude
among the non-diabetic group.
Baseline amplitude of the right and left abductor pollicis brevis (APB), tibialis anterior
(TA), abductor hallucis (AH) and quadriceps (QUAD) were compared with the closing
amplitude of the right and left abductor pollicis brevis (APB), tibialis anterior (TA), abductor
hallucis (AH) and quadriceps (QUAD) of the same group. The table below is displaying paired
T-test applied for L-APB, L-TA and R-AH. Paired T-test was used because we were analyzing
difference with data which was not time series but had means, two groups, interdependent
samples and normal distribution. Wilcoxon Signed Rank test was applied for R-APB, R-TA,
L-AH, R-QUAD and L-QUAD because we were analyzing difference for the data which was
not time series but have means, two groups, interdependent samples and non-normal
distributed. We rejected the null hypothesis and accepted alternative hypothesis for all muscle
groups because of P ? (0.05).
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Table 10: Non-Diabetic MEPs amplitude difference:
MEPs Amplitude (µ?) Difference Baseline Vs Closing
Non-Diabetic Group
Mean St Dev Normal
ity Test
P-
Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
R-APB Baseline 142.5 16.41 0.030 Wilcoxon
Signed
Rank
M= 7.250
P – Value
0.02
0.77% P ; ? = H1
R-APB Closing 143.6 17.74 0.007
L-APB Baseline 145.6 32.74 0.069 Paired T-
test
T= -2.35
P – Value
0.037
1.03 % P ; ? = H1
L-APB Closing 147.1 34.45 0.063
R-TA Baseline 125.4 42.16 0.006 Wilcoxon
Signed
Rank
M= 7.250
P – Value
0.002
0.55% P ; ? = H1
R-TA Closing 126.1 42.37 0.009
L-TA Baseline 113.0 41.18 0.162 Paired T-
test
T= – 2.90
P – Value
0.013
0.44% P ? = Ho
R-AH Closing 101.9
53.96 0.270
L-AH Baseline 121.7 55.79 0.019 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
-0.82% P ; ? = H1
L-AH Closing 120.7 58.30 0.019
R-QUAD Baseline 89.44 53.76 0.011 Wilcoxon
Signed
Rank
M= 7.250
P – Value
0.002
0.98% P ; ? = Ho
R-QUAD Closing 90.32 52.78 0.009
L-QUAD Baseline 101.8 35.43 0.005 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
0.39% P ; ? = H1
L-QUAD Closing 102.2 35.52 0.005
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9.2- Non-diabetic group MEPs onset latency (OL):
Null hypothesis (Ho) = There is no difference between baseline and closing onset latency of
MEPs among the non-diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing onset
latency among the non-diabetic group.
Baseline onset latency of the right and left abductor pollicis brevis (APB), tibialis
anterior (TA), abductor hallucis (AH) and quadriceps (QUAD) were compared with the closing
onset latency of the right and left abductor pollicis brevis (APB), tibialis anterior (TA),
abductor hallucis (AH) and quadriceps (QUAD) of the same group. The table below is
exhibiting that paired T-test applied for R-APB, R-TA and L-TA. Paired T-test was used
because we were analyzing difference with data which was not time series but had means, two
groups, interdependent samples and normal distribution. Wilcoxon Signed Rank test was
applied for L-APB, R-AH, L-AH, R-QUAD and L-QUAD because we were analyzing
difference for the data which was not time series but have means, two groups, interdependent
samples and non-normal distributed. We rejected the null hypothesis and accepted alternative
hypothesis for R-APB, L-APB, L-TA, L-AH, R-QUAD and L-QUAD because of P ? (0.05).
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Table 11: Non-Diabetic MEPs onset latency difference:
MEPs Onset Latency (ms) Difference Baseline Vs Closing
Non-Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
R-APB Baseline 22.84 3.020 0.373 Paired T-
test
T= – 2.80
P – Value
0.016
0.39% P ; ? = H1
R-APB Closing 22.93 2.996 0.431
L-APB Baseline 23.22 3.803 0.005 Wilcoxon
Signed
Rank
M= 6.750
P – Value
0.002
0.43 % P ? = Ho
R-TA Closing 28.75 5.536 0.070
L-TA Baseline 27.72 3.807 0.060 Paired T-
test
T= – 2.55
P – Value
0.025
0.43% P ? = Ho
R-AH Closing 36.69
8.339 0.006
L-AH Baseline 36.48 6.468 0.037 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
9.40% P ; ? = H1
L-AH Closing 33.05 4.921 0.012
R-QUAD Baseline 24.42 4.535 0.028 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
2.66% P ; ? = H1
R-QUAD Closing 25.07 4.906 0.025
L-QUAD Baseline 22.44 5.445 0.005 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
0.76% P ; ? = H1
L-QUAD Closing 22.61 5.388 0.005
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10. Question 6: Difference between baseline and closing MEPs among the
Diabetic group?
P-value was used to define the results when P ? (0.05) we believed on null
hypothesis (Ho) which was there is no difference.
10.1- Diabetic group MEPs amplitude (amp):
Null hypothesis (Ho) = There is no difference between baseline and closing amplitude of MEPs
among the diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing amplitude
among the diabetic group.
Baseline amplitude of the right and left abductor pollicis brevis (APB), tibialis anterior
(TA), abductor hallucis (AH) and quadriceps (QUAD) were compared with the closing
amplitude of the right and left abductor pollicis brevis (APB), tibialis anterior (TA), abductor
hallucis (AH) and quadriceps (QUAD) of the same group. The table below is displaying paired
T-test applied to all muscle group. Paired T-test was used because we were analyzing
difference with data which was not time series but had means, two groups, interdependent
samples and normal distribution. We rejected the null hypothesis and accepted alternative
hypothesis for all right and left muscle group because of P ; ? (0.05).
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Table 12: Diabetic group MEPs amplitude difference:
MEPs Amplitude (µ?) Difference Baseline Vs Closing
Diabetic Group
Mean St Dev Normality
Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
R-APB Baseline 149.7 43.85 0.172 Paired T-
test
T= 3.91
P – Value
0.002
-5.47% P ; ? = H1
R-APB Closing 141.5 44.22 0.156
L-APB Baseline 150.5 44.57 0.261 Paired T-
test
T= 3.88
P – Value
0.002
-2.32% P ; ? = H1
L-APB Closing 147.0 44.27 0.176
R-TA Baseline 156.8 51.08 0.277 Paired T-
test
T= 2.53
P – Value
0.026
-4.46% P ; ? = H1
R-TA Closing 149.8 50.66 0.249
L-TA Baseline 158.9 46.44 0.285 Paired T-
test
T= 3.58
P – Value
0.004
-2.58% P ; ? = H1
L-TA Closing 154.8 46.16 0.244
R-AH Baseline 152.0 64.97 0.157 Paired T-
test
T= 2.03
P – Value
0.045
-13.49% P ; ? = H1
R-AH Closing 131.5 53.42 0.301
L-AH Baseline 151.3 58.31 0.084 Paired T-
test
T= 4.77
P – Value
0.000
-1.78% P ; ? = H1
L-AH Closing 148.6 59.06 0.062
R-QUAD Baseline 123.1 36.15 0.169 Paired T-
test
T= 5.76
P – Value
0.000
-2.35% P ; ? = H1
R-QUAD Closing 120.2 35.40 0.162
L-QUAD Baseline 132.9 43.85 0.230 Paired T-
test
T= 4.28
P – Value
0.001
-2.63% P ; ? = H1
L-QUAD Closing 129.4 43.73 0.171
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10.2- Diabetic group MEPs onset latency (OL):
Null hypothesis (Ho) = There is no difference between baseline and closing onset latency of
MEPs among the diabetic group.
Alternative hypothesis (H?) = There is the difference between baseline and closing onset
latency among the diabetic group.
Baseline onset latency of the right and left abductor pollicis brevis (APB), tibialis
anterior (TA), abductor hallucis (AH) and quadriceps (QUAD) were compared with the closing
onset latency of the right and left abductor pollicis brevis (APB), tibialis anterior (TA),
abductor hallucis (AH) and quadriceps (QUAD) of the same group. Wilcoxon Signed Rank
test was applied to all muscle groups except R-AH because we were analyzing difference for
the data which was not time series but have means, two groups, interdependent samples and
non-normal distributed. Paired T-test was applied for R-AH because we were analyzing
difference with data which was not time series but had means, two groups, interdependent
samples and normal distribution. We rejected the null hypothesis and accepted alternative
hypothesis for all right and left muscle group because of P ; ? (0.05).
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Table 13: Diabetic group MEPs onset latency difference:
MEPs Onset Latency (ms) Difference Baseline Vs Closing
Diabetic Group
Mean St Dev Normali
ty Test
P- Value
Statistical
Test
P-Value of
Statistical
Test
% Change
In Amplitude
baseline Vs
Closing
Significance
P ? = Ho
R-APB Baseline 23.84 7.049 0.005 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
3.02% P ; ? = H1
R-APB Closing 24.56 7.061 0.005
L-APB Baseline 23.45 7.001 0.005 Wilcoxon
Signed
Rank
M= 6.750
P – Value
0.002
2.86% P ; ? = H1
L-APB Closing 24.12 7.050 0.005
R-TA Baseline 30.99 6.183 0.277 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
2.69% P ; ? = H1
R-TA Closing 31.82 6.630 0.024
L-TA Baseline 29.04 4.667 0.020 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.004
2.31% P ; ? = H1
L-TA Closing 29.71 4.618 0.019
R-AH Baseline 32.56 6.270 0.427 Paired T-
test
T= -13.78
P – Value
0.000
2.05% P ; ? = H1
R-AH Closing 33.23 6.321 0.336
L-AH Baseline 33.95 5.098 0.013 Wilcoxon
Signed
Rank
M= 7.250
P – Value
0.002
8.95% P ; ? = H1
L-AH Closing 36.99 6.561 0.126
R-QUAD Baseline 24.30 7.788 0.005 Wilcoxon
Signed
Rank
M= 7.00
P – Value
0.002
2.88% P ; ? = H1
R-QUAD Closing 25.00 7.736 0.005
L-QUAD Baseline 24.57 8.162 0.005 Wilcoxon
Signed
Rank
M= 6.750
P – Value
0.002
2.65% P ; ? = H1
L-QUAD Closing 25.22 8.109 0.005
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11. Question 7: Can Diabetes Mellitus lead to increase in onset latency and
decrease in amplitude during intraoperative monitoring of scoliosis
correction surgery?
P-value was used to define the results when P ? (0.05) we believed on null
hypothesis (Ho) which was there is no difference.
Null hypothesis (Ho) = Diabetes Mellitus cannot lead to decrease in amplitude (µV) during
intraoperative monitoring of scoliosis correction surgery.
Alternative hypothesis (H?) = Diabetes Mellitus can lead to decrease in amplitude (µV) during
intraoperative monitoring of scoliosis correction surgery.
Null hypothesis (Ho) = Diabetes Mellitus cannot lead to increase in onset latency (ms) during
intraoperative monitoring of scoliosis correction surgery.
Alternative hypothesis (H?) = Diabetes Mellitus can lead to increase in onset latency (ms)
during intraoperative monitoring of scoliosis correction surgery.
Amplitude and onset latency of both right and left median and posterior tibial nerves
was compared between non-diabetic and diabetic groups to find out the difference. Likewise,
amplitude and onset latency of both right and left abductor pollicis brevis (APB), tibialis
anterior (TA), abductor hallucis (AH) and quadriceps (QUAD) were compared between non-
diabetic and diabetic groups. The table below is illustrating that Mann-Whitney test was
applied for the amplitude of MEPs and onset latency of both SSEPs and MEPs because we
analyzed difference for the data which was not time series, had means, independent samples
and two groups but either data had non-normal distribution or insignificant Levene’s variance
test. Two sample tests were applied for the amplitude of SSEPs because we analyzed difference
for the data with means, two groups, independent samples, equal variance and normal
distribution. We rejected the null hypothesis for both amplitude (µV) and onset latency (ms).
We accepted the alternative hypothesis (H?) as stated erstwhile. So, diabetes mellitus could
increase the onset latency (ms) as well as could decrease the amplitude (µV) for both upper
and lower limbs during intraoperative monitoring (SSEPs & MEPs) of scoliosis correction
surgery because of P < ? (0.05).
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Table 14: Comparison of SSEPs and MEPs among the Non-Diabetic and Diabetic group:
Comparison of SSEPs and MEPs among a Non-Diabetic and Diabetic group
Mean St Dev Normality
Test
P- Value
Equal
variance
Levene’s
Test
Statistical
Test
P-Value of
Statistical
Test
Significance
P ? = Ho
Non-Diabetic
SSEPs
Amplitude (µ?)
2.569 2.038
0.215
Vs
P-Value
0.064
Two
Sample
T-Test
T= 19.89
P – Value
0.000
P ; ? = H1
Diabetic SSEPs
Amplitude (µ?)
-13.85 1.138 0.589
Non-Diabetic
MEPs
Amplitude (µ?)
0.635 0.3205 0.789 P-Value
0.174
Mann
Whitney
Test
W=100
P – Value
0.0009
P ; ? = H1
Diabetic MEPs
Amplitude (µ?)
-4.385 3.884 0.005
Non-Diabetic
SSEPs
Onset Latency (ms)
0.5625 0.5813 0.146 P-Value
0.000
Mann
Whitney
Test
W= 36
P – Value
0.0009
P ; ? = H1
Diabetic SSEPs
Onset Latency (ms)
5.579 3.417 0.063
Non-Diabetic
MEPs
Onset Latency (ms)
1.813 3.170 0.005 P-Value
0.713
Mann
Whitney
Test
W=47
P – Value
0.0313
P ; ? = H1
Diabetic MEPs
Onset Latency (ms)
3.462 2.255 0.005
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12. Percentage change in SSEPS amplitude:
The graph below is depicting the percentage change in somatosensory evoked
potentials (SSEPs) amplitude monitored from the right and left median (RMN ; LMN) and
posterior tibial nerves (RTN ; LTN) throughout the scoliosis correction surgery among the
diabetic and non-diabetic group. Blue bars are demonstrating percentage increase in amplitude
from the baseline among non-diabetic patients. Orange bars are signifying percentage decrease
in amplitude from the baseline among diabetic patients. Negative (-) sign is indicating a
reduction in amplitude among diabetic patients.
Figure 23: Bar chart for the percentage change is SSEPs amplitude among both groups.
4.10%4.46%
0.70%1.03%
-12.45%
-13.95%-14.92%-14.09%
-20.00%
-15.00%
-10.00%
-5.00%
0.00%
5.00%
10.00%
RMNLMNRTNLTN
% Change in SSEPS amplitude among diabetic and non-diabetics
during the scoliosis surgery
N-DMDM
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13. Percentage change in SSEPs onset latency:
The graph below is portraying the percentage change in somatosensory evoked
potentials (SSEPs) onset latency monitored from the right and left median (RMN ; LMN) and
posterior tibial nerves (RTN ; LTN) throughout the scoliosis correction surgery among the
diabetic and non-diabetic group. Blue bars are indicating percentage increase in onset latency
from the baseline among non-diabetic patients. Orange bars are signifying percentage increase
in onset latency from the baseline among diabetic patients.
Figure 24: Bar chart for the percentage change in SSEPs onset latency among groups.
0.74%
1.35%
0.12%0.08%
7.52%
9.79%
2.72%2.30%
0.00%
2.00%
4.00%
6.00%
8.00%
10.00%
12.00%
RMNLMNRTNLTN
% Change in SSEPs onset latency among diabetics and non-diabetics
during the scoliosis surgery
N-DMDM
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14. Percentage Change in MEPs amplitude:
The graph below is illustrating the percentage change in motor evoked potentials
(MEPs) amplitude monitored from right and left abductor pollicis brevis (R-APB ; L-APB),
tibialis anterior (R-TA ; L-TA), abductor hallucis (R-AH ; L-AH) and quadriceps (R-QUAD
; L-QUAD) throughout the scoliosis correction surgery among diabetic and non-diabetic
group. Blue bars are indicative of the percentage increase and decrease in amplitude from the
baseline among non-diabetic patients. Orange bars are signifying percentage decrease in
amplitude from the baseline among diabetic patients. Negative (-) sign is indicating a decline
in amplitude.
Figure 25: Bar chart for the percentage change in MEPs amplitude among groups.
0.77%1.03%0.55%0.44%-0.10%-0.82%
0.98%
0.39%
-5.47%
-2.32%
-4.46%
-2.58%
-13.49%
-1.78%-2.35%-2.63%
-16.00%
-14.00%
-12.00%
-10.00%
-8.00%
-6.00%
-4.00%
-2.00%
0.00%
2.00%
R-APBL-APBR-TAL-TAR-AHL-AHR-QUADL-QUAD
% Change in MEPs amplitude among diabetics and non-diabetics
during scoliosis surgery
Non-Diabetic GroupDiabetic Group
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15. Percentage change is MEPs onset latency:
The graph below is illustrating the percentage change in motor evoked potentials
(MEPs) onset latency monitored from right and left abductor pollicis brevis (R-APB ; L-
APB), tibialis anterior (R-TA ; L-TA), abductor hallucis (R-AH ; L-AH) and quadriceps (R-
QUAD ; L-QUAD) throughout the scoliosis correction surgery among diabetic and non-
diabetic group. Blue bars are indicative of the percentage increase in onset latency from the
baseline among non-diabetic patients. Orange bars are signifying percentage increase in onset
latency from the baseline among diabetic patients.
Figure 26: Bar chart for the percentage change in MEPs onset latency among groups.
0.39%0.43%0.21%0.43%0.22%
9.40%
2.66%
0.76%
3.02%2.86%2.69%
2.31%2.05%
8.95%
2.88%
2.65%
0.00%
1.00%
2.00%
3.00%
4.00%
5.00%
6.00%
7.00%
8.00%
9.00%
10.00%
R-APBL-APBR-TAL-TAR-AHL-AHR-QUADL-QUAD
% Change in MEPs onset latency among diabetics and non-diabetics
during scoliosis surgery
Non-Diabetic GroupDiabetic Group
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SECTION-IV
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DISCUSSION:
Many authors already reported the adverse effect of the diabetes mellitus on the sensory
and motor peripheral nerves. In this study, statistical results proved that diabetes mellitus could
increase the onset latency and decrease the amplitude of somatosensory and motor evoked
potentials (SSEPs ; MEPs) significantly among diabetic patients during scoliosis surgery as
compared to the non-diabetic patients during scoliosis surgery. It was found that
somatosensory and motor evoked potentials are always susceptible to minor changes during
scoliosis surgery irrespective of diabetes mellitus, but these changes are not significant
clinically as well as statistically. Baseline somatosensory and compound motor nerve action
potentials (SNAP ; CMAP) recorded before the commencement of the scoliosis surgery were
compared with closing somatosensory, and motor evoked potentials recorded after the closure
of the skin for both diabetic and non-diabetic groups. Statistical analysis was done by using
Wilcoxon Signed Rank and Paired T-test. P-value of the statistical test and % change in
amplitude ; onset latency between baseline and closing somatosensory evoked potentials were
used to define the results.
It was found that right median nerve somatosensory evoked potentials (RMN-SSEPs)
amplitude was decreased by 12.45% among diabetic patients and it was increased by 4.10%
among non-diabetic patients at the level of closure. Onset latency (OL) of the right median
nerve somatosensory evoked potentials (RMN-SSEPs) was increased by 7.52% among
diabetic patients and 0.74% among non-diabetic patients. Similarly, left median nerve
somatosensory evoked potentials (LMN-SSEPs) amplitude was decreased by 13.95% among
the diabetic group, and it was increased by 4.46% among the non-diabetic group. Although,
left median nerve somatosensory evoked potentials (LMN-SSEPs) onset latency (OL) was
increased 9.79% among diabetic patients and 1.35% among non-diabetic patients. Likewise,
right posterior tibial nerve somatosensory evoked potentials (RTN-SSEPs) amplitude was
decreased by 14.92% among diabetic individuals, and it was increased by 0.70% among non-
diabetic individuals. Though, right posterior tibial nerve somatosensory evoked potentials
(RTN-SSEPs) onset latency (OL) was increased 2.72% among diabetic patients and 0.12%
among non-diabetic patients. Correspondingly, left posterior tibial nerve somatosensory
evoked potentials (LTN-SSEPs) amplitude was decreased by 14.09% among the diabetic
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group, and it was increased by 1.03% among the non-diabetic group. However, left posterior
tibial nerve somatosensory evoked potentials (LTN-SSEPs) onset latency (OL) was increased
2.30% among diabetic patients and 0.08% among non-diabetic patients.
Motor evoked potentials (MEPs) analysis revealed that amplitude of the right abductor
pollicis brevis (R-APB) was decreased by 5.47% among diabetic patients and it was increased
by 0.77% among non-diabetic patients. Onset latency (OL) of the right abductor pollicis brevis
(R-APB) was increased by 3.02% among diabetic patients and 0.39% among non-diabetic
patients. Similarly, left abductor pollicis (L-APB) motor evoked potentials amplitude was
decreased 2.32% among diabetics, and it was increased by 1.03% among non-diabetics.
Though, onset latency (OL) of left abductor pollicis brevis (L-APB) was increased by 2.86%
among diabetic groups and 0.43% among non-diabetic groups. In the same way, the right
tibialis anterior (R-TA) motor evoked potentials amplitude was decreased 4.46% among the
diabetic group, and it was increased by 0.55% among the non-diabetic group. Although, onset
latency (OL) of the right tibialis anterior (R-TA) was increased by 2.69% among diabetic
individuals and 0.21% among non-diabetic individuals. Correspondingly, the left tibialis
anterior (L-TA) motor evoked potentials amplitude was decreased by 2.58% among diabetic
patients, and it was increased by 0.44% among non-diabetic patients. And onset latency of the
left tibialis anterior (L-TA) was increased by 2.31% and 0.43% among diabetic and non-
diabetic patients respectively.
In the same manner, the right abductor hallucis (R-AH) motor evoked potential
amplitude was decreased to 13.49% among the diabetic group, and it was reduced by 0.10%
among the non-diabetic group. Onset latency (OL) of the right abductor hallucis was increased
2.05% among diabetic patients and 0.22% among non-diabetic patients. Likewise, left abductor
hallucis (L-AH) motor evoked potentials amplitude was decreased by 1.78% among diabetic
individuals, and it was reduced by 0.82% among non-diabetic individuals. Onset latency (OL)
of the left abductor hallucis (L-AH) was a quiet variable than the other muscle groups. It was
increased by 8.95% among people with diabetes and 9.40% among non-diabetics. Motor
evoked potentials amplitude of the right quadriceps (R-QUAD) was decreased to 2.35% among
diabetic patients, and it was increased by 0.98% among non-diabetic patients. And onset
latency (OL) of right quadriceps (R-QUAD) was increased by 2.88% among people with
diabetes and 2.66% among non-diabetics. Correspondingly, the left quadricep (L-QUAD)
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motor evoked potentials amplitude was decreased 2.63% among a diabetic group of patients,
and it was increased by 0.39% among a non-diabetic group of the patients. Onset latency (OL)
of the left quadriceps (L-QUAD) rose 2.65% among a diabetic group of patients and 0.76%
among non-diabetic groups of the patients.
Generally, the amplitude of the both somatosensory evoked potentials (SSEPs) and
motor evoked potentials (MEPs) were decreased among a diabetic group of the patients as
compared to the non-diabetic group of the patients. The amplitude of the sensory and motor
action potentials (SNAP ; CMAP) reflects the number of the active conducting nerve and
muscle fibres. Amongst diabetic patient’s extra body glucose is get deposited into the nerves
and muscles. This glucose damage the active nerve and muscle fibres which can ultimately
cause peripheral neuropathy and muscle weakness. It can be the reason for the reduction in
amplitude among diabetic patients during scoliosis surgery. Likewise, onset latency (OL) of
somatosensory and motor evoked potentials (SSEPs and MEPs) was increased among both
diabetic and non-diabetic groups. But, this increase in onset latency was significantly high
among diabetics than non-diabetic patients. Onset latency (OL) represents the speed of
conduction of the sensory and motor nerves. Increase in onset latency represents slow
conduction of the sensory and motor nerves. The probable reason behind the similar behaviour
of both groups may be because of anaesthesia or scoliosis surgery itself. Anaesthesia can
increase the onset latency by slowing down transmission of the nerve impulse, and scoliosis
surgery can also cause mild to moderate compression on peripheral nerves leading to
increasing onset latency. In the diabetic patients’ elevated levels of the glucose damage the
myelin sheath of the nerves by depositing extra glucose inside the nerves and muscles
ultimately slowing the nerve impulse transmission and conduction velocity. Secondly, diabetes
affects the blood vessels which can reduce blood supply to the nerve and muscles leading to
slow transmission of the nerve impulse. Possibly, this can be the reason behind the significant
increase in onset latency among diabetic patients as compared to non-diabetic patients.
The results we discussed earlier were only for either diabetics or non-diabetics. After
that, we linked the differences of somatosensory and motor evoked potentials (SSEPs ; MEPs)
by comparing amplitude and onset latency of the diabetic group with the amplitude and onset
latency of the non-diabetic group. Mann Whitney and Two-Sample T-test was used for this
analysis, and it was found P-value of the somatosensory and motor evoked potentials amplitude
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and onset latency was lower than the value of alpha (? = 0.05). It means there is that diabetes
mellitus can lead to increase in onset latency and decrease in amplitude during intraoperative
monitoring of scoliosis correction surgery. These results were very consistent with the work of
Arrthy S, and colleagues. They compared median nerve somatosensory evoked potentials
(MN-SSEPs) between diabetic and non-diabetic patients. They measured the onset latency
(OL) and central conduction time (CCT) of both groups and applied an unpaired T-test on the
mean values. P-value of the statistical test was less than alpha (? = 0.05) for diabetic patients.
They concluded that the diabetic group had prolonged central conduction time due to delayed
central and peripheral nerve conduction as compared to the non-diabetic group (Arrthy et al.,
2014).
Frequently, during spinal cord correction surgeries, e.g. scoliosis, alarming criteria for
somatosensory and motor evoked potentials is decreased in the amplitude of more than 50%
and an increase in onset latency or peak latency of more than 10%. For motor evoked potentials
all or none criteria is also used. Patients meeting these criteria during correction surgeries
usually presents with a neurological deficit after surgery if undetected or untreated on the spot.
Many scientists were mostly comfortable with somatosensory evoked potentials (SSEPs). We
monitored both somatosensory and motor evoked potentials (SSEPs and MEPs) in this study
because together their sensitivity and specificity was 100% and 98% respectively (Marafona
and Machado, 2018). We found that diabetes caused a significant reduction in amplitude and
a substantial increase in onset latency among diabetic groups as compared to the non-diabetic
group, but these findings were quite below than the alarming criteria. Every single patient from
both groups was examined after the surgery for any neurological deficit, but no patient was
reported with any neurological shortfall.
Hyun Mi oh and colleagues also found a comparable conclusion to this study. They
related median nerve somatosensory evoked potentials (MN-SSEPs) bilaterally among
diabetic and non-diabetic patients. They measured cortical and inter-peak latencies of both
groups and analysed data statistically. They found that the P-value of the statistical test was
less than alpha (? = 0.05) for diabetic patients. So, they summarised that N20 cortical latency
and N20-P25 peak latencies were significantly increased among diabetic patients as compared
to the non-diabetics. The central conduction time was also meaningfully increased among
diabetic patients (Oh et al., 2015). Another author Dr Manoj Kumar and his colleagues
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evaluated the effect of diabetes on the evoked potentials. He compared the brainstem auditory
evoked potentials (BAEPs) among diabetic and non-diabetic patients. He measured the wave
onset and interpeak latency and analysed the mean values statistically. He found that interpeak
and onset latencies of the brainstem auditory evoked potentials were significantly increased
among diabetic patients than non-diabetic patients (Jain et al., 2018).
Effect of diabetes on the peripheral nerves was evaluated by Hikmet Dolu and
colleagues. Their results were also like this study. They monitored multimodal evoked
potentials bilaterally from two groups of patients named as diabetic and non-diabetic.
Somatosensory evoked potentials (SSEPs) were recorded from the median and posterior tibial
nerve along with brainstem evoked potentials (BAEPs) and visual evoked potentials (VEPs).
They also monitored the motor evoked potentials (MEPs). They compared Peripheral, cortical,
interpeak latencies and central motor conduction time between diabetic and non-diabetic
groups. They found that visual evoked potentials latencies and peripheral and central latencies
for median nerve and posterior tibial nerves were prolonged among the diabetic group.
Brainstem auditory evoked potentials were remained normal in diabetics. Central conduction
time and latency of the motor evoked potentials were also increased. So, they concluded that
duration and severity of diabetes cause peripheral and central neuropathies (Dolu et al., 2003).
Results of this study were also very consistent with an earlier study by Giuseppe
Pozzessere, MD who evaluated the different modalities among diabetic and non-diabetic
patients. He monitored multimodal evoked potentials, somatosensory evoked potentials
(SSEPs) from the median and posterior tibial nerves, brainstem auditory evoked potentials
(BAEPs) and visual evoked potentials (VEPs). He measured the latencies from all different
modalities and analysed mean values statistically. He found a significant reduction in
conduction velocity and a momentous increase in the latencies among most of the modalities
(Pozzessere et al., 1988). Jin Jun Luo and colleagues also did a comparative study with multiple
modalities. They measured onset latencies from somatosensory evoked potentials (SSEPs),
visual evoked potentials (VEPs) and brainstem evoked potentials. They analysed the data by
comparing the mean values and found a significant reduction in central conduction velocity of
the somatosensory evoked potentials but no noteworthy change in conduction velocity of the
visual and brainstem auditory evoked potentials (Luo et al., 2015).
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Effects of diabetes mellitus on the somatosensory and motor evoked potentials (SSEPs
; MEPs) during spinal cord surgery together were infrequently studied. Most of the authors
were more focused on somatosensory evoked potentials (SSEPs), and they were very
constrained by the onset or interpeak latencies as pronounced earlier. None of them either
examined latencies and amplitude difference of the motor evoked potentials (MEPs) neither
amplitude difference of somatosensory evoked potentials (SSEPs). Pavol Kucera and
colleagues went one step further and studied the effect of the diabetes mellitus on the spinal
cord lesions by investigating somatosensory and motor evoked potentials to prevent the side
effects of diabetes in patients with spinal cord injuries. They divided the patients into two
groups named as diabetic and control group. They stimulated the median and ulnar nerve from
upper limb and fibular nerve from lower limb for somatosensory evoked potentials (SSEPs)
and measured latencies from each nerve.
Similarly, they also stimulated the first dorsal interosseous muscle and extensor
digitorum brevis for motor evoked potentials (MEPs) latencies. They analyzed the data and
found that diabetes caused prolonged peripheral and central conduction time. They confirmed
that somatosensory and motor evoked potentials could be used for endorsement of
imperceptible lesion of the spinal cord among diabetic patients. Results of our study were also
very parallel with the findings of Pavol Kucera and colleagues because we also measure onset
latencies from both somatosensory and motor evoked potentials. We also related the results
between the diabetic group and non-diabetic group. We found that diabetes increased onset
latency significantly among diabetic group than the non-diabetic group and caused prolonged
peripheral and conduction time (Kucera et al., 2005).
Piotr Rajewski and colleagues concluded the very similar results to this study. They
only included diabetic patients and then divided sample size according to gender, type of
diabetes, glycemic control and peripheral polyneuropathy. They monitored somatosensory
evoked potentials (SSEPs) and visual evoked potentials (VEPs). Median and posterior tibial
nerves were used for somatosensory evoked potentials. They noted onset and peak latencies
and worked out central conduction time for each modality. They found that 25% of patients
with prolonged somatosensory latencies and central conduction times without signs of
polyneuropathy. They also observed that 64.4% of patients with abnormal somatosensory
latencies and central conduction times and 31.1% with visual evoked potentials abnormalities.
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So, They concluded that evoked potentials examination could detect subclinical changes
among diabetic patients (Rajewski et al., 2007).
A scientist Ping-Hui Wang and colleagues studied the effect of diabetes on the
decompression spinal cord surgeries by recording somatosensory and motor evoked potentials
(SSEPs and MEPs) in the rats. Their findings of SSEPs and MEPs on rats’ model were also
alike in this study. They compared Streptozotocin-induced diabetic rats with sciatic nerve
compression with the non-diabetic rats with sciatic nerve compression. They measured the
amplitude and onset latency of somatosensory and motor evoked potentials (SSEPs and MEPs)
and analysed the data with the Kruskal-Wallis test. They noticed that compression of the sciatic
nerve caused significant reduction of amplitude and increase in onset latency of both
somatosensory and motor evoked potentials and these findings were more significant among
diabetic rats’ group. Decompression surgery was performed, and they monitored the SSEPs
and MEPs and found that both SSEPs and MEPs were significantly improved among both
groups. They measured SSEPs and MEPs again after eight weeks and founded that non-
diabetic rats’ functions were normal but diabetic groups SSEPs and MEPs were not recovered.
So, they summarised that decompression surgery is effective among diabetics, but complete
recovery is not possible (Wang et al., 2017).
Critical evaluation of the results of this study with all previous studies reflected that the
results of this study were very reliable and even more detailed because patients were strictly
examined for selection criteria and allocated into diabetic and non-diabetic groups. Amplitude
and onset latencies were measured from both somatosensory and motor evoked potentials
(SSEPs and MEPs) data before commencement of the surgery as a baseline and after the
closure of the skin as a closing potential. Data were analyzed statistically as well as clinically,
and results were given in the form of tables and graph which can be easily understood. Now,
as we found that diabetes does affect amplitude and onset latency, but these variations are not
clinically noteworthy. So, these results will be helpful to prevent false alarms during spinal
cord surgical procedure among diabetic patients, to facilitate the surgical procedure precisely,
and to plan the postoperative management according to the neuromuscular status of the nerve
and muscles.
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Limitations:
Even though almost every possible effort was made to justify the criteria for this study,
but there are still some methodical concerns. The first limitation of this study was sample size
was too small. It was difficult to find the patients with both variables (diabetes and scoliosis)
together because both conditions are not common together. The second limitation of this study
was that data was taken from a single hospital setting due to the shortage of the time. This
study should be completed within the three-month period. Another possible constraint for the
study is that we only appraised the effect of diabetes on only one type of spinal cord surgery
(Scoliosis), which can reduce the specificity and sensitivity of this study. The last limitation of
this study was the design of the study. This study was a retrospective cohort study in which
data was taken from previous surgeries. The drawback of this type of study was we had less
control over variables, and to some extent, this design is susceptible to information or recall
bias.
Recommendation:
Further studies are required to find out the effect of diabetes on somatosensory and
motor evoked potentials (SSEPs and MEPs) during scoliosis correction surgery. This study
can be amended by varying the study design from a retrospective cohort study to either
prospective cohort study or randomized control trial. This will increase the level of the
evidence for this study. A sample size of the study can be improved by repeating this study at
a bigger level with a greater number of the patients in both diabetic and non-diabetic group so
more accurate results can be found. Data can be collected from more than one hospital settings
or even from more than one country at the international level which will increase the sample
size as well as the level of evidence. Effect of diabetes on spinal cord operations can be
measured more precisely by including numerous surgical procedures in the study e.g. spinal
cord tumours, ankylosing spondylitis and other degenerative spinal cord problems and
recording both somatosensory and motor evoked potentials from upper and lower limbs.
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CONCLUSION:
Diabetic neuropathy is one of the foremost complications of the diabetes mellitus. It’s
a major microvascular problem which affects diabetic patients and causes hitches in central,
peripheral and autonomic nervous systems. Patients with scoliosis deformity and diabetes are
more prone to get these problems. Many studies attempted to find out the effect of diabetes on
the patients with spinal cord lesions. This study was also carried out to comprehend the
consequence of diabetes mellitus on the peripheral nerves and spinal cord in scoliosis surgery
during intraoperative monitoring so postoperative management can be planned accordingly.
Baseline somatosensory and motor evoked potentials (SSEPs ; MEPs) amplitude of the non-
diabetic group was compared with the closing amplitude of the same group, and it was found
that amplitude was slightly increased (0.39% to 4.46%) at the end of the surgery. On the other
side, when baseline amplitude of the both somatosensory and motor evoked potentials (SSEPs
; MEPs) of diabetic patients were compared with the closing amplitude of the same group, it
was found that amplitude was significantly decreased (-1.78% to -14.92%) at the end of the
surgery. As it was reflected by the preceding studies that diabetes cause irreversible damage to
the conduction fibres and motor units. Our results evidenced this declaration as we found a
consistent decrease in amplitude. Likewise, baseline onset latency (OL) of somatosensory and
motor evoked potentials (SSEPs ; MEPs) was compared with closing onset latency (OL) for
both non-diabetic and diabetic groups, and it was noted that onset latency was increased among
both diabetic and non-diabetic groups. But, this increase in onset latency was significantly high
among diabetics than non-diabetic patients. These results were very consistent and identical to
the findings of the earlier studies. The aim of the study was approached by equating the
differences in amplitude and onset latencies between diabetic and non-diabetic groups. It was
found that the P-value of the somatosensory and motor evoked potentials (SSEPs ; MEPs)
amplitude and onset latency were lower than the value of alpha (? = 0.05). So, we concluded
that diabetes does affect amplitude and onset latency, but these variations are not clinically
noteworthy. These results will be helpful clinically to prevent false alarms during spinal cord
surgical procedure among diabetic patients, to facilitate the surgical procedure precisely, and
to plan the postoperative management according to the neuromuscular status of the nerve and
muscles.
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SECTION-V
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SECTION-VI
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APPENDIX-I: MIDDLESEX UNIVERSITY ETHICAL FORM:
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APPENDIX-II: GHURKI TRUST TEACHING HOSPITAL ETHICAL
REVIEW COMMITTEE (ERC) CERTIFICATE:
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APPENDIX-III: SSEPs and MEPs raw data:
Table 15: Median Nerve SSEPs raw data:
Non-Diabetic: Median Nerve SSEPs N20/P25 ms Diabetic: Median Nerve SSEPs N20/P25 ms
Baseline Closing Baseline Closing
RMN RMN LMN LMN RMN RMN LMN LMN RMN RMN LMN LMN RMN RMN LMN LMN
C3-Fpz C3-C4 C4-Fpz C4-C3 C3-Fpz C3-C4 C4-Fpz C4-C3 Cz-Fpz C4-C3 Cz-Fpz C3-C4 Cz-Fpz C4-C3 Cz-Fpz C3-C4
Amp µ? 5.3 5.2 5.1 4.8 5.2 5.8 5.2 5.1 2.1 4.0 2.3 1.7 2.0 3.8 2.1 1.3
OL ms 12.5 12.7 11.6 11.8 12.4 12.5 11.7 11.9 12.8 12.6 13.5 12.5 13.4 12.8 13.7 12.6
Amp µ? 4.3 4.0 4.4 3.0 4.6 4.2 4.9 3.2 1.6 1.6 0.8 0.8 1.3 1.4 0.7 0.8
OL ms 14.1 13.3 13.4 10.2 14.2 13.2 13.1 10.6 12.3 11.6 11.0 10.7 12.6 11.9 11.4 11.3
Amp µ? 3.9 3.5 3.3 1.7 4.8 3.7 3.8 2.1 2.8 3.0 2.3 2.9 2.7 2.8 2.0 2.8
OL ms 14.4 14.7 12.8 11.4 14.5 14.5 13.0 12.1 15.4 14.1 13.5 13.8 15.7 16.3 15.6 16.2
Amp µ? 3.9 3.6 3.8 3.3 4.0 3.9 3.8 3.9 2.3 2.1 2.0 2.4 1.4 1.2 1.3 1.8
OL ms 14.5 13.9 13.8 14.0 14.7 14.2 14.1 14.4 14.0 14.2 13.8 13.8 15.5 15.7 15.1 15.0
Amp µ? 3.5 3.1 3.2 3.1 3.6 3.2 3.1 3.3 3.5 3.1 5.5 4.7 3.2 2.8 4.1 4.2
OL ms 13.2 13.3 13.3 12.9 13.3 13.5 13.4 13.2 15.5 14.3 14.8 14.0 16.8 15.5 16.3 15.9
Amp µ? 4.0 3.2 3.8 3.1 4.2 3.5 3.9 3.3 3.2 3.5 4.1 4.4 3.0 3.2 3.7 3.9
OL ms 16.5 16.8 14.3 14.6 16.3 16.7 14.5 14.3 13.5 13.3 13.6 13.8 14.4 14.2 14.3 14.7
Amp µ? 4.6 4.4 4.7 4.9 4.5 4.4 4.8 4.8 1.7 1.3 1.9 1.8 1.2 0.9 1.4 1.3
OL ms 16.7 16.6 14.8 15.3 16.7 16.5 15.0 15.2 18.5 18.8 18.7 19.2 21.7 22.0 22.6 23.4
Amp µ? 4.3 3.8 3.9 4.1 4.3 3.9 4.4 4.2 2.4 2.6 2.9 3.2 2.0 2.1 2.3 2.8
OL ms 14.0 14.6 14.5 14.8 14.1 14.5 14.5 14.8 16.2 15.7 16.1 16.3 17.1 16.9 17.8 17.6
Amp µ? 4.8 4.6 4.0 4.2 5.0 4.9 4.0 4.3 4.2 3.2 2.9 2.5 3.6 2.8 2.5 2.0
OL ms 17.9 17.4 16.9 18.0 18.1 17.4 17.0 17.8 15.6 15.3 16.0 15.6 16.3 16.1 16.9 16.3
Amp µ? 4.5 4.7 4.6 4.8 4.6 4.7 4.5 5.0 3.0 3.6 3.5 3.4 2.4 2.9 3.0 2.8
OL ms 16.8 15.9 16.5 16.9 17.1 16.0 16.7 17.3 18.7 17.8 17.6 18.6 21.3 19.4 20.4 22.1
Amp µ? 4.6 4.4 4.6 4.5 4.5 4.4 4.7 4.8 2.9 2.8 3.6 3.1 2.8 2.6 3.4 2.8
OL ms 18.7 17.3 18.2 18.0 19.5 18.2 19.0 18.7 13.7 12.8 15.0 15.1 14.4 13.9 15.7 16.0
Amp µ? 6.5 5.4 6.6 6.0 6.5 5.7 6.7 6.3 1.9 2.3 2.8 2.9 2.1 2.3 2.9 2.9
OL ms 20.8 18.8 16.4 15.6 21.1 19.1 16.7 16.0 17.1 18.0 17.9 17.4 17.5 18.8 18.6 18.9
Amp µ? 3.9 3.3 3.7 3.3 4.1 3.6 3.7 3.4 4.0 2.8 2.4 2.3 3.7 2.4 2.1 2.0
OL ms 15.8 14.2 13.3 14.5 15.8 14.3 13.5 14.5 15.7 16.5 15.8 15.4 16.3 17.1 16.6 16.1
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Table 16: Posterior Tibial Nerve SSEPs raw data:
Non-Diabetic: Tibial Nerve SSEPs N8/P37 ms Diabetic: Tibial Nerve SSEPs N8/37 ms
Baseline Closing Baseline Closing
RTN RTN LTN LTN RTN RTN LTN LTN RTN RTN LTN LTN RTN RTN LTN LTN
Cz-Fpz C4-C3 Cz-Fpz C3-C4 Cz-Fpz C4-C3 Cz-Fpz C3-C4 Cz-Fpz C4-C3 Cz-Fpz C3-C4 Cz-Fpz C4-C3 Cz-Fpz C3-C4
Amp µ? 3.8 4.5 3.9 3.8 4.0 4.6 4.1 3.9 3.8 3.4 5.2 3.1 3.3 3.0 4.9 2.8
OL ms 17.9 19.3 18.3 19.5 18.0 19.5 18.6 19.6 21.0 27.5 26.8 28.3 23.8 28.3 27.1 28.9
Amp µ? 4.5 4.7 4.2 4.0 4.6 4.7 4.3 4.2 1.6 1.4 3.3 0.8 1.3 1.4 2.7 0.8
OL ms 25.5 25.2 27.0 27.8 25.4 25.3 27.1 27.6 20.3 21.0 18.2 19.8 20.6 21.4 18.8 20.3
Amp µ? 4.0 3.4 3.6 2.8 4.1 3.4 3.8 2.7 2.9 3.1 3.1 2.5 2.7 2.8 2.6 2.4
OL ms 28.5 27.2 25.3 26.2 28.7 27.4 25.0 26.1 29.7 30.5 29.3 30.2 30.3 31.1 29.9 30.8
Amp µ? 4.1 3.9 3.8 3.3 4.0 3.9 3.8 3.6 2.5 2.3 2.1 2.4 1.7 1.6 1.3 1.8
OL ms 31.8 30.7 31.3 31.2 31.7 30.7 31.2 31.2 28.4 28.1 29.0 28.8 29.4 28.8 29.7 29.3
Amp µ? 3.7 3.3 3.5 3.2 3.6 3.2 3.3 3.4 3.2 3.5 5.6 4.9 3.0 3.1 4.9 4.2
OL ms 28.3 27.7 26.6 25.3 28.2 27.6 26.6 25.5 28.7 28.4 29.1 28.5 29.3 28.9 29.8 29.1
Amp µ? 4.4 3.8 4.0 3.9 4.3 3.5 3.9 3.8 3.5 3.7 4.2 4.4 3.0 3.3 3.7 3.9
OL ms 30.1 30.3 29.7 29.4 30.3 30.1 29.5 29.5 31.1 30.7 29.3 29.8 31.8 31.5 30.1 30.6
Amp µ? 4.7 4.8 4.9 5.1 4.6 4.8 5.0 5.0 1.9 1.5 2.1 2.0 1.3 1.1 1.7 1.4
OL ms 28.4 28.6 28.9 29.1 28.4 28.5 29.0 29.1 29.9 30.1 29.4 29.8 30.7 30.9 30.1 30.6
Amp µ? 4.0 3.5 3.7 3.9 4.1 3.5 3.7 3.9 2.1 2.6 2.6 3.0 1.8 2.3 2.2 2.8
OL ms 27.7 28.1 27.3 27.6 27.5 28.0 27.3 27.5 29.3 28.4 29.1 29.0 29.9 28.7 29.6 29.5
Amp µ? 4.8 4.6 4.0 4.2 5.0 4.7 4.0 4.3 3.8 3.6 3.1 2.9 3.0 2.9 2.7 2.3
OL ms 17.9 17.4 16.9 18.0 18.1 17.4 17.0 17.8 24.1 26.3 25.7 26.2 24.8 26.9 26.3 27.0
Amp µ? 4.6 4.4 4.6 4.3 4.6 4.5 4.6 4.2 3.1 3.5 3.6 3.7 2.4 2.9 3.0 2.8
OL ms 26.8 25.9 26.5 26.9 26.8 26.1 26.6 26.8 28.7 27.8 28.6 28.6 29.3 29.4 29.4 29.1
Amp µ? 4.9 4.8 4.7 4.6 4.8 4.7 4.6 4.5 3.9 3.8 3.6 3.7 3.1 2.9 2.8 3.1
OL ms 25.7 26.3 25.2 26.0 25.5 26.2 25.0 25.7 27.7 28.8 28.0 28.1 28.5 29.3 28.7 28.9
Amp µ? 6.5 5.4 6.6 6.0 6.5 5.7 6.7 6.3 1.9 2.3 2.8 2.9 2.1 2.3 2.9 2.9
OL ms 20.8 18.8 16.4 15.6 21.1 19.1 16.7 16.0 27.1 28.0 27.9 27.4 27.8 28.7 28.5 28.0
Amp µ? 3.9 3.3 3.7 3.3 4.1 3.6 3.7 3.4 4.0 2.8 2.4 2.3 3.7 2.4 2.1 2.0
OL ms 25.8 24.2 24.3 24.5 25.8 24.3 24.5 24.5 31.2 30.8 29.9 30.5 31.7 31.4 30.7 31.2
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Table 17: MEPs amplitude (µ?) raw data:
Non-Diabetic: MEPs Amplitude (µ?) Diabetic: MEPs Amplitude (µ?)
Right Left Right Left
APB TA AH QUAD APB TA AH QUAD APB TA AH QUAD APB TA AH QUAD
Baseline 165.7 166.1 24.5 25.3 186.9 98.8 46.2 84.5 123.1 156.1 79.0 65.2 131.3 146.2 84.2 67.4
Closing 171.2 169.0 25.2 30.2 192.3 99.4 47.3 86.1 99.8 127.2 67.1 62.5 122.3 133.8 78.5 60.2
Baseline 135.1 78.1 74.8 37.9 174.4 76.0 180.1 63.1 203.1 225.5 237.1 139.8 209.3 219.5 221.0 189.5
Closing 136.2 79.3 72.1 38.2 178.2 77.2 182.1 62.6 194.1 218.1 231.1 134.0 201.4 212.4 218.3 179.5
Baseline 117.5 52.7 45.2 26.9 99.8 47.1 26.5 40.0 87.4 73.2 71.0 87.1 84.3 79.5 73.2 89.2
Closing 117.9 53.0 45.5 27.1 100.2 47.5 27.0 40.2 84.1 72.3 69.2 85.9 82.1 77.9 71.7 88.0
Baseline 136.4 59.7 64.1 67.7 135.1 51.3 63.4 65.3 158.3 146.9 159.3 150.8 147.0 175.5 175.9 146.9
Closing 136.1 59.9 64.2 67.9 135.0 51.3 63.5 65.4 152.2 144.5 156.0 148.8 145.8 172.5 173.7 144.4
Baseline 174.4 167.9 170.2 158.9 160.5 179.5 173.3 131.1 204.4 228.4 234.2 138.6 207.3 216.4 220.1 179.5
Closing 174.2 168.2 171.0 159.0 161.0 181.1 172.9 131.5 199.9 225.3 132.1 135.4 203.5 214.3 218.5 176.6
Baseline 138.3 142.2 122.0 140.3 112.1 139.2 134.2 132.1 112.1 123.4 114.3 117.4 119.3 125.4 119.3 121.2
Closing 138.4 142.4 122.4 140.4 112.4 139.4 134.4 132.4 110.2 121.3 111.1 113.4 115.2 123.4 113.4 119.4
Baseline 127.2 135.5 149.4 130.3 129.7 133.3 140.5 129.2 184.2 173.2 199.1 168.2 185.1 174.4 189.5 167.2
Closing 127.0 135.1 149.5 130.9 128.8 132.9 141.2 130.0 173.2 167.3 188.8 163.1 182.5 171.2 187.6 163.3
Baseline 147.7 145.5 174.6 92.2 182.8 138.0 163.8 131.1 116.2 134.2 139.4 123.3 118.4 136.2 140.2 117.2
Closing 148.2 145.7 175.0 93.2 183.1 138.7 164.2 131.8 117.3 135.1 140.4 124.0 119.2 137.1 141.0 118.3
Baseline 133.4 153.4 158.4 139.4 126.6 152.3 159.3 134.9 87.4 73.2 71.0 87.1 84.3 79.5 73.2 89.2
Closing 133.0 153.0 158.0 139.0 126.2 152.0 159.0 134.5 84.1 72.3 69.2 85.9 82.1 77.9 71.7 88.0
Baseline 165.7 166.1 24.5 25.3 186.9 98.8 46.2 84.5 204.4 228.4 234.2 138.6 207.3 216.4 220.1 179.5
Closing 171.2 169.0 25.2 30.2 192.3 99.4 47.3 86.1 199.9 225.3 132.1 135.4 203.5 214.3 218.5 176.6
Baseline 138.3 142.2 122.0 140.3 112.1 139.2 134.2 132.1 123.1 156.1 79.0 65.2 131.3 146.2 84.2 67.4
Closing 138.4 142.4 122.4 140.4 112.4 139.4 134.4 132.4 99.8 127.2 67.1 62.5 122.3 133.8 78.5 60.2
Baseline 138.3 142.2 122.0 140.3 112.1 139.2 134.2 132.1 184.2 173.2 199.1 168.2 185.1 174.4 189.5 167.2
Closing 138.4 142.4 122.4 140.4 112.4 139.4 134.4 132.4 173.2 167.3 188.8 163.1 182.5 171.2 187.6 163.3
Baseline 135.1 78.1 74.8 37.9 174.4 76.0 180.1 63.1 158.3 146.9 159.3 150.8 147.0 175.5 175.9 146.9
Closing 136.2 79.3 72.1 38.2 178.2 77.2 182.1 62.6 152.2 144.5 156.0 148.8 145.8 172.5 173.7 144.4
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Table 18: MEPs onset latency (OL) raw data:
Non-Diabetic: MEPs Latency (ms) Diabetic: MEPs Latency (ms)
Right Left Right Left
APB TA AH QUAD APB TA AH QUAD APB TA AH QUAD APB TA AH QUAD
Baseline 20.8 38.8 36.2 26.2 19.3 25.8 35.2 19.8 23.2 34.1 35.4 22.1 24.1 33.6 33.4 23.2
Closing 21.0 38.7 36.0 30.2 19.2 26.0 35.0 20.0 24.1 34.9 36.2 22.8 24.9 34.2 33.9 23.8
Baseline 20.3 23.5 38.3 22.3 19.0 26.5 36.8 19.7 19.0 22.2 30.0 17.0 17.3 23.0 34.3 17.0
Closing 20.5 23.3 38.5 22.5 19.2 26.7 40.0 19.9 19.5 22.8 30.7 17.9 17.8 23.6 34.8 17.7
Baseline 25.8 28.3 42.7 21.0 27.2 30.8 44.3 17.0 39.3 36.3 34.2 40.7 38.4 32.3 34.1 41.7
Closing 25.7 28.4 42.9 21.1 27.3 31.0 44.4 17.3 40.0 37.0 35.1 41.3 39.1 33.0 34.9 42.2
Baseline 26.7 32.2 45.5 24.0 26.9 33.0 45.2 24.1 21.0 33.8 40.8 21.3 20.7 29.3 38.7 20.3
Closing 26.8 32.4 45.3 24.1 27.1 33.3 45.4 24.4 21.8 34.3 41.3 21.9 21.4 30.0 29.5 20.9
Baseline 22.2 30.3 39.3 21.8 25.2 32.7 43.2 31.2 22.5 24.7 31.1 19.2 19.9 24.4 33.1 18.8
Closing 22.3 30.4 39.5 21.9 25.1 32.8 43.1 31.1 23.1 25.3 31.7 19.7 20.4 25.0 33.8 19.3
Baseline 24.2 23.4 19.1 33.4 26.1 22.9 24.1 31.2 19.2 23.4 24.5 22.1 19.8 24.1 24.9 22.4
Closing 24.3 23.7 19.5 33.2 26.4 22.7 24.5 31.3 20.0 25.2 24.9 22.9 20.5 25.0 25.5 23.3
Baseline 16.8 23.8 35.5 23.5 18.3 24.3 36.0 18.2 20.8 42.3 40.3 28.2 20.3 34.9 44.0 28.2
Closing 16.7 23.7 35.4 23.4 18.2 24.2 35.5 18.1 21.3 42.9 41.1 28.9 20.8 35.4 44.7 28.9
Baseline 22.3 26.5 37.5 18.2 21.3 25.3 36.0 18.7 23.2 34.1 35.4 22.1 24.1 33.6 33.4 23.2
Closing 22.5 26.7 37.7 18.4 21.5 25.5 36.2 18.9 24.1 34.9 36.2 22.8 24.9 34.2 33.9 23.8
Baseline 20.8 38.8 36.2 26.2 19.3 25.8 35.2 19.8 23.2 34.1 35.4 22.1 24.1 33.6 33.4 23.2
Closing 21.0 38.7 36.0 30.2 19.2 26.0 35.0 20.0 24.1 34.9 36.2 22.8 24.9 34.2 33.9 23.8
Baseline 20.3 23.5 38.3 22.3 19.0 26.5 36.8 19.7 19.0 22.2 30.0 17.0 17.3 23.0 34.3 17.0
Closing 20.5 23.3 38.5 22.5 19.2 26.7 40.0 19.9 19.5 22.8 30.7 17.9 17.8 23.6 34.8 17.7
Baseline 25.8 28.3 42.7 21.0 27.2 30.8 44.3 17.0 39.3 36.3 34.2 40.7 38.4 32.3 34.1 41.7
Closing 25.7 28.4 42.9 21.1 27.3 31.0 44.4 17.3 40.0 37.0 35.1 41.3 39.1 33.0 34.9 42.2
Baseline 26.7 32.2 45.5 24.0 26.9 33.0 45.2 24.1 21.0 33.8 40.8 21.3 20.7 29.3 38.7 20.3
Closing 26.8 32.4 45.3 24.1 27.1 33.3 45.4 24.4 21.8 34.3 41.3 21.9 21.4 30.0 29.5 20.9
Baseline 24.2 23.4 19.1 33.4 26.1 22.9 24.1 31.2 19.2 23.4 24.5 22.1 19.8 24.1 24.9 22.4
Closing 24.3 23.7 19.5 33.2 26.4 22.7 24.5 31.3 20.0 25.2 24.9 22.9 20.5 25.0 25.5 23.3
