Burst Stimulation

Disclaimer
This presentation contains information on products that are undergoing
clinical evaluation and are not FDA approved. The presentation is not
meant to make any claims that these products have been found safe or
effective by FDA.
The ProdigyTM system has received CE Mark in March 2014

Outline
Chronic Pain Overview
Prevalence and cost burden
How is pain perceived? Central mechanisms & psychology of pain

Unmet needs in SCS for chronic pain management

Non-response / inadequate response at trial

Patient intolerance of paresthesia, further compounded by patient positionality
Evolving pain patterns post-implant of permanent SCS system
Address patients pre-occupation with pain

Burst Stimulation
How well does it target unmet needs Clinical evidence review
How does Burst stimulation work mechanisms of action
Open questions and evidence generation

Prevalence and Costs Associated with Chronic Pain

Prevalence
Chronic pain affects more than 1.5 billion people worldwide1

About 100 million in the U.S. 2

Estimated 19% of adult Europeans3

Cost Burden
Economic impact of chronic pain is greater than most other health conditions
due to absenteeism, reduced productivity, and increased risk of leaving labor
market3
Costs the U.S. billions of dollars in health care and lost work productivity each year 2
In Denmark, an estimated 1 million working days have been lost annually 5 with productivity costs
accounting for 85% of the total lower back pain costs per patient 6

Lower back pain is among the top 10 diseases and injuries that account for
the highest number of disability-adjusted life-years worldwide4

1.
2.
3.
4.
5.
6.

Boorsook D, Cerebrum June 2012

Relieving Pain in America, Institute of Medicine of the National Academies, June 2011
Phillips CJ. British Journal of Pain 2009.
Lim SS, et al. The Lancet 2012.
Eriksen J, et al. Pain 2006
Eriksen J, et al. Pain 2003

How is pain perceived?

SENSORY

Intensity,
Localization,
Discrimination

CONTEXT
Pain Beliefs,
Expectation,
Placebo

Pain
Experience

Depression,
Catastrophising,
Anxiety

CHEMICAL &
STRUCTURE

COGNITIVE

Hypervigilance,
Attention,
Distraction,
Catastrophising

Neurodegeneration
Metabolic
(e.g. opioidergic,
dopaminergic)
Maladaptive Plasticity

Nociceptive
Modulation
5

* Psychological and Neural Mechanisms of the Affective Dimension of

Pain, Price et al, Science, 00368075, Vol.288, Issue 5472

MOOD

A or C
Nociceptive
input

Somatosensory System
(Price 2000, Craig 2002, Fields 2004, Rainville 1999)

Perception &
Discrimination

Lateral System

Consciousness

Affective
& Attention

Medial System

Emotion

Impact of psychological factors in pain experience 1

Nociceptive
Stimulus

Attention

Boundaries:
Culture, Family

Emotional

Interpretation

Cognitive

Coping Strategy

Behavior
Feedback
Situation

Consequences

1 Linton SJ and WS Shaw. Impact of psychological factors in the experience of pain.

Physical Therapy. 2011; 91: 700-711.

Positive

Negative

Learning

Impact of Psychological Factors in the Experience of Pain1

Factor

Description

Possible Effect on Pain

Attention

Pain demands patients attention

Vigilance may increase pain intensity

Distraction may decrease pain intensity

Cognition

How patient thinks about pain

Interpretations and beliefs may increase pain

Catastrophizing may increase pain
Negative thoughts and beliefs may
increase pain
Cognitive sets may reduce flexibility in
dealing with pain

Emotions and
emotion
regulation

Pain often generates negative

feelings, which subsequently may
influence the pain and fuel
cognitions, attention, and overt
behaviors

Fear may increase avoidance behavior

Depression and anxiety may increase pain
Distress fuels negative cognitions and pain
Positive emotions might decrease pain

Overt behavior

What patients do to cope with pain

influences perception

Avoidance behavior may increase disability

Overactivity may provoke pain
Pain behaviors communicate pain

1 Linton SJ and WS Shaw. Impact of psychological factors in the experience of

pain. Physical Therapy. 2011; 91: 700-711.

Studies consistently show decreases in gray matter

in patients with chronic pain1,2,3
Imaging studies have shown that
chronic pain is associated with
changes in the brain:
Patients with chronic back pain
have significantly less gray matter
volume than control patients1,2
mainly in the brainstem and
somatosensory cortex2
CRPS patients exhibit regional
gray matter atrophy, localized
white matter anisotropy, and
changes in branching in
connectivity of white matter tracts3

1. Apkarian AV, et al. J Neuroscience 2004.

2. Schmidt-Wilcke T, et al. Pain 2006.

3. Geha PY, et al. Neuron 2008.

Altered brain
chemistry
Decrease in gray
matter volume

Altered brain
network connectivity

Structural changes
in nerve tracts

Chronic pain results in altered behaviors

Sensory (e.g. spontaneous pain at rest)
Affective (e.g. anxiety, depression, suicide, addiction)
Cognitive (e.g. decreased attention)
Emotional (e.g. reward deficit state)
Image adapted from Boorsook D. Cerebrum 2012.

Time to intervention post diagnosis of pain matters

Accompanying psychological factors and structural changes in the brain may result in a
differential benefit depending on time of intervention from diagnosis of pain 1
100%
90%
80%
70%
60%

Success Rate (%)

50%

Failure
Success

40%
30%
20%
10%
0%
<2

2 to 5

5 to 8

8 to 11

11 to 15

Time Until Intervention (years)

10

1 Kumar K, et al. Spinal cord stimulation in treatment of chronic benign pain: challenges in treatment planning
and present status, a 22-year experience. Neurosurgery 2006 March;58(3):481-96; discussion 481-96.

> 15

Unmet needs in SCS for

chronic pain management

Concept of SCS
Neuropathic pain
Ectopic or spontaneous discharges in C fibres
(Wu 2002)

Paresthesia and dysesthesia

Ectopic discharges in A fibres
(Ochoa 1980, Nordin 1984)

Spinal cord stimulation

Activates A to suppress C and A fibers
Via inhibitory interneurons (Melzack & Wall 1965)

12

1.

Cui et al., Neuroscience Letters, 1998.

Inadequate pain control with tonic SCS trials

SCS for neuropathic pain is an accepted standard of care in the
treatment of chronic pain. However, current solutions may not fully
address patients pre-occupation with pain or other associated
psychological factors
With increasing awareness and quantification, studies now show 2030% of patients are non-responders*1,2, with some studies showing
even higher rates of failed trials3.
Pain control in patients with nociceptive pain remains ineffective 4,5
*Non-Responders defined as:
i) All failed trials
ii) Permanent cases w/ insufficient pain coverage over time
iii) Complex back pain (severe intensity) inadequately addressed with tonic stimulation

13

1. Vancamp T, et al. INS 2013

2. Truin M, Janssen SP, van Kelef M, Joosten EA. Eur J Pain. 2011
3. Lad et al, A National Survey of Spinal Cord Stimulation Trial to Permanent Conversion Rates , NANS 2013 poster
4. Raphael et al, Spinal Cord Stimulation and its Anesthetic Implications, Continuing Education in Anesthesia,
Critical Care and Pain (CEACCP), Volume 9, No.3, 2009
5. Krames E, Implantable devices for pain control: spinal cord stimulation and intrathecal therapies, Best Pract Res
Clin Anaesthesiology 2002 Dec;16(4):619-49.

Paresthesia is a challenging component of tonic

SCS therapy1
Tonic SCS (above perception threshold) relies on the
presence of paresthesia in treated limbs to:
Deliver pain reduction using Gate theory
Validate appropriate lead positioning

This aspect of the modality has some limitations:

Obtaining paresthesia in the lower back can be challenging
(despite numerous technical improvements).
Changes in body position can significantly modify intensity of
paresthesia requiring frequent adjustments.
Substantial minority of patients do not tolerate paresthesia,
or prefer not to feel sensation at all.

Painful or undesirable paresthesia is a reported reason

for failed SCS trials.

14

1. Oakley JC, Spinal Cord Stimulation in Axial Low Back Pain: Solving the Dilemma, Pain Medicine, Vol 7, No. S1, 2006

Inadequate pain control or dislike for SCS therapy are most

common reasons for withdrawal after trial period
Approximately 25% of patients withdraw after the SCS implant trial period1
Approximately 69% of withdrawing patients cited inadequate or dislike for
SCS therapy1
In some studies, approximately 15% of patients underwent explantation of
SCS systems2
Approximately 25% of patients refuse permanent SCS implants1

25%

Reasons for refusing permanent SCS implant1

31%
69%

75%

Withdrawn

15

Permanent implant

Inadequate or dislike of SCS therapy

Other

1. Oakley JC, et al. A new spinal cord stimulation system effectively relieves chronic, intractable pain: a multicenter
prospective clinical study. Neuromodulation 2007; 10(3): 262-278..
2. Mekhail et al, Cost Benefit of Neurostimulation for Chronic Pain, Clin f Pain Volume 20, Number 6,
November/December 2004

Understanding BURST stimulation

Spinal Cord Stimulation Waveforms

Traditional Tonic

Relatively low energy

Recharge every 1-2 months

Burst Stimulation

Parameters within traditional

ranges
Low-moderate energy
Average recharge similar to tonic
Device provides both tonic & burst1
Same expected device life as
tonic1

High Frequency Stimulation

19

1 ProdigyTM Clinician Manual, referenced 5/5/2014

2 - Nevro Corp. 10186-ENG-Physician Manual Rev G. 2012. Menlo
Park, CA, USA

Parameters outside the traditional ranges

Highest energy, daily recharge
Device only provides tonic stimulation at
programmable frequencies (up to
10,000hz) 2
Reduced device life compared to tonic 2

Understanding Neuron Types: Tonic versus Burst

Some neurons fire in a tonic

or continuous manner

Other neurons fire in groups of action potentials

(bursts) followed by periods of dormancy

Both burst & tonic firing neurons may be parallel firing modes within the same sensory system 1
Composition of burst & tonic firing neurons varies in the pain pathway thereby creating a need
for tailored therapy
20

1. Oswald AM, et al. J Neurosci. 2004.

Differences in Burst and Tonic Neuronal Signals

There is a non-linear response to burst signals in the cortex
Burst is a start & stop signal that overrides the tonic pain stimuli
and creates stronger signal in cortex than tonic signals

Cortical Cell
Visual Repsonse

Visual Repsonse

60
EPSPs

40

Spikes

20

burst
Sherman 2001

0.5

Signal

21

1.

1.0

Noise

1.5

2.0

Time(s)

0.5

1.0

1.5

2.0

Thalamic Relay Cell

Sherman S.M. A wake-up call from the thalamus. Nature Neuroscience. 2001; 4(4):344-346

Origins of Burst Stimulation

Burst is a naturally occurring signaling modality in human
physiology and is interpreted differently by the nervous
system1,2,3.
e.g. Thalamic cells can fire in tonic and burst modes1.

Thalamic burst firing considered a more potent activator of

the cortex2,3. Ascending action potentials more likely to be
routed to the cortex when thalamic cells firing in bursts.

22

1. Jahnsen H, Llins R. : Voltage-dependent burst-to-tonic switching of thalamic cell activity: an in vitro study. Arch Ital Biol. 1984 Mar;122(1):73-82.
2. Harvey A. Swadlow & Alexander G. Gusev : The impact of 'bursting' thalamic impulses at a neocortical synapse. Nature Neuroscience 4, 402 - 408 (2001).
3. Sherman SM : A wake-up call from the thalamus. Nature neuroscience, 2001

Current Working Hypothesis:

Burst stimulation may exert its main effect through an
ability to modulate both lateral & medial pathways
Pain stimuli are likely processed in parallel by two pathways:
Lateral discriminatory pathway helps identify the location, type
and intensity of pain
Hybrid pathway consisting of
WDR neurons firing in tonic PH (lam. 1, 4-6) Thalamus (VPL, VPM)
1 & 2 SSC. Predominant triggering neurons in the lateral pathway
Low-threshold neurons firing in burst can also be found in the lateral pathway

Medial affective/attentional pathway helps drive attention &

salience to the pain
Nociceptive specific neurons firing in bursts PH (lam. 1)
Thalamus (MDvc, VMpo) Anterior Cingulate, Anterior Insula,
Amygdala.
Fires in bursts2.

23

1.
2.
3.

De Ridder D, et al. World Neurosurgery 2013.

Lopez-Garcia JA, and AE King. Eur J Neuroscience 1994.
Larry R. Squire, Darwin Berg, Floyd E. Bloom, Sascha du Lac, Anirvan Ghosh, Nicolas C. Spitzer. Fundamental
Neuroscience. 3rd Edition, Chapter 25: Somatosensory System, Academic Press (Elsevier), p. 599,2008.

Source-localized EEG supports significantly more

alpha activity in medial pathway

In a subgroup of 5 patients in
De Ridders study, burst
stimulation showed more alpha
activity in the dorsal anterior
cingulate in comparison with
tonic, placebo, and baseline.

24

De Ridder, et al. World Neurosurgery 2013

fMRI study suggests thalamus and ACC are

responsive to SCS stimulation and modulating
pain perception

25

Moens M, et al. Neuroradiology 2012.

First Steps in Understanding Burst and Paresthesia

Burst does not send information through the tactile pathway1.
Wide Dynamic Range Neurons Pain & Tactile
50

Neuronal Activity (imp/s)

50

40

Before
SCS

30
NS

10

* p<0.05
26

40
Neuronal Activity (imp/s)

Before SCS
During SCS

30

20

Low Threshold Tactile Neurons

NS

20

10

0
Tonic SCS

Burst SCS

Tonic SCS

* p<0.05

1 Tang, R., Martinez, M., Goodman-Keiser, M., Farber, J. P., Qin, C., & Foreman, R. D. (2013). Comparison of
Burst and Tonic Spinal Cord Stimulation on Spinal Neural Processing in an Animal Model. Neuromodulation:
Technology at the Neural Interface, n/a-n/a. doi: 10.1111/ner.12117

Burst SCS

Patient benefit
from concept to evidence

Burst Stimulation suppressed pain with no paresthesia

reported in 83% of tested patients
7

First study to report on Burst Stimulation

for suppression of neuropathic pain
(n=12).
All patients underwent implantation of SJM
Lamitrode paddle lead and Eon IPG
Average follow-up time of 20.5 months

6
5
4

preoperative
tonic
burst

VAS3 Pain
2

Key takeaways:
17% of patients experienced parasthesia
following burst stimulation vs. 92% of
patients following tonic stimulation
Burst stimulation resulted in a significant
improvement of 7.29 VAS points postoperatively for limb pain (p < 0.001)
Burst stimulation also resulted in
significant improvement on the McGill
Short Form, 16.73 points from preoperative experience (p<0.001)
No complications or adverse events
reported

1
0

axial

De Ridder D et al. Neurosurgery 2010.

limb right

20
18
16
14
12

preoperative
tonic
burst

10

McGill
8
6
4
2
0

sensory
28

limb left

affective

Burst stimulation is superior over tonic stimulation

for suppressing pain
Primary Outcome: % VAS Improvement vs. Baseline
80%

70%

Secondary Outcome: % Improvement in PVAQ vs. Baseline

12%

* p<0.05

10%

* p<0.05 vs. placebo and tonic

*
*

60%

8%

6%

50%

4%

40%

*
2%

30%

0%
20%

-2%
10%

-4%
0%
Back pain

Placebo
29

Limb Pain

Tonic

General Pain

Burst

De Ridder, et al. World Neurosurgery 2013

[N=15 patients, trialed for 1 week each with
Placebo, Tonic & Burst stimulation modes]

-6%

Attention to pain

Placebo

Attention to changes in pain

Tonic

Burst

Burst stimulation improves pain relief and is preferred by

FBSS patients over tonic or placebo stimulation
Purpose: To evaluate the effectiveness of Burst Stimulation compared to
placebo and Tonic (500 Hz) stimulation (n=20)
Pain intensity and pain quality scores were significantly decreased with Burst
Stimulation compared to other treatment groups:
Primary outcome: Mean NRS (pain intensity) for Burst Stimulation: 4.72.5
Mean SFMPQ (pain quality) for Burst Stimulation: 19.910.5
No significant differences between ODI categories

Burst Stimulation was preferred in 80% (16/20) of the patients

9
8
7
6
5
NRS4
3
2
1
0

7.1
1.9

500 Hz

30

4.7
2.5

Burst

Schu S, et al. NANS 2013.

8.3
1.1

Placebo

28.6
19.9
10.2 10.5

9
8
7
6
5
SFMPQ
4
3
2
1
0

500 Hz

Burst

33.5
11.8

Placebo

9
8
7
6
5
ODI4
3
2
1
0

24.6
19.2
7.3 8.8

500 Hz

Burst

29.5
10.3

Placebo

Burst stimulation may salvage non-responders and

improve response in tonic SCS responders

102 patients at 2 centers

23.5% of patients did not respond to tonic SCS therapy
62.5% of chronic non-responders to tonic SCS responded to Burst stimulation
94.9% of chronic responders to tonic SCS had further improvement to response
rate with Burst stimulation
Implants
(n=102)

Non-responders
23.5%

Burst responders
62.5%

31

1.

Vancamp T, et al. INS 2013

Burst

Failures
37.5%

Tonic

Responders
76.5%

Improvement
with Burst
94.9%

Burst

Non-improvement
5.13%

Burst stimulation provides further pain relief in patients first

treated with tonic stimulation
General pain VAS scores
* p<0.001 vs. baseline
# p<0.05 vs. baseline
p<0.05 vs. tonic

*
Average VAS scores
*

Baseline
32

100
90
80
*
70
60
50 *
40
30
20
10
0

Tonic stimulation

de Vos CC, et al. Neuromodulation 2013.

Compared to baseline, burst

stimulation resulted in:
77% reduction in VAS scores in
diabetic neuropathy patients
57% reduction in VAS scores in failed
back syndrome (FBSS) patients
23% reduction in VAS scores in
FBSS patients who were poor
responders over time to tonic
stimulation

In comparison to tonic stimulation,

about 60% of patients experienced
further pain reduction when burst
stimulation was applied

Burst stimulation

Ongoing Clinical Experience1

200+ patients at 9 centers utilizing modified
SJM Eon Mini rechargeable IPG
Burst Stimulation compares favorably to tonic
and may even rescue some tonic failures
95% of Tonic responders have greater pain
relief with Burst Stimulation
60%-80% of Tonic non-responders respond
to Burst Stimulation thereby reducing
therapy failures.
Paresthesia is minimized with burst
stimulation.

A multicenter study on tonic and burst spinal cord stimulation

(Unpublished data)
10
9
8
7
6
Visual 5analog Scale
4
3
2
1
0
Belgium
baseline

The Netherlands
tonic stimulation

10
9
8
7
6
5
4
3
Visual2analog Scale

4.0
3.5
3.0
2.5
Visual Analogue Scale 2.0

1
0

1.5
1.0
0.5
0.0

33

1 Data on file

burst stimulation

Burst stimulation as a back-up for failures of tonic spinal cord stimulation (Unpublished data)

Sensation of paresthesia
(Unpublished data)
4.5

At visit

Placebo

Total

Tonic

Burst

Burst stimulation

Clinical experience & evidence with BURST continues

to evolve
SUNBURST IDE:
Large pre-market IDE trial with 116 patients at 20 sites
Currently enrolling
Compares both safety & efficacy of BURST stimulation in comparison
with standard SCS tonic stimulation
ProdigyTM PMCF study:
European post-market study highlighting long-term safety and efficacy
of BURST stimulation utilizing ProdigyTM SCS systems from SJM
123 patients at 20 sites; 12 months follow-up

34

References
1.
2.
3.
4.
5.
6.
7.
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27.
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29.
30.
31.
32.
33.
34.
35.
36.
37.

36

Borsook D. A Future Without Chronic Pain: Neuroscience and Clinical Research. Cerebrum. 2012 May-Jun: 7.
Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Institute of Pain Medicine. June 2011.
Phillips CJ. The cost and burden of chronic pain. British Journal of Pain 2009. 3(1): 2-5.
Lim SS, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 19902010: a systematic analysis for the Global Burden of
Disease Study 2010. The Lancet, Vol 380, Issue 9859, Pages 2224-2260. 15 December 2012.
Eriksen J, et al. Critical issues on opiods in chronic non-cancer pain: An epidemiological study. Pain 2006; 125: 172-9.
Eriksen J, et al. Epidemiology of chronic non-malignant pain in Denmark. Pain 2003; 106: 221-8.
Price et al. Psychological and Neural Mechanisms of the Affective Dimension of Pain. Science, 00368075, Vol.288, Issue 5472
Price 2000 (somatosensory system)
Craig 2002 somatosensory system
Fields 2004 somatosensory system
Rainville 1999 somatosensory system
Linton SJ et al. Impact of psychological factors in the experience of pain. Physical Therapy. 2011; 91: 700-711
Apkarian AV, et al. Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. J Neuroscience 2004. 24(46): 10410-10415.
Schmidt-Wilcke T, et al. Affective components and intensity of pain correlate with structural differences in gray matter in chronic back pain patients. Pain 2006. 125: 89-97.
Geha PY, et al. The brain in chronic CRPS pain: Abnormal gray-white matter interactions in emotional and autonomic regions. Neuron 2008. 60: 570-581.
Kumar K, et al. Spinal cord stimulation in treatment of chronic benign pain: challenges in treatment planning and present status, a 22-year experience. Neurosurgery 2006 March;58(3):481-96; discussion
481-96.
Cui et al., Neuroscience Letters, 1998
Vancamp T, et al. Preliminary Outcomes With A New Stimulation Design: Response Comparison And Budget Impact Modelling. INS 2013.
Truin M, et al. Eur J Pain. 2011
Lad et al, A National Survey of Spinal Cord Stimulation Trial to Permanent Conversion Rates , NANS 2013 poster
Raphael et al, Spinal Cord Stimulation and its Anesthetic Implications, Continuing Education in Anesthesia, Critical Care and Pain (CEACCP), Volume 9, No.3, 2009
Krames E, Implantable devices for pain control: spinal cord stimulation and intrathecal therapies, Best Pract Res Clin Anaesthesiology 2002 Dec;16(4):619-49.
Oakley JC, Spinal Cord Stimulation in Axial Low Back Pain: Solving the Dilemma, Pain Medicine, Vol 7, No. S1, 2006
Oakley JC, et al. A new spinal cord stimulation system effectively relieves chronic, intractable pain: a multicenter prospective clinical study. Neuromodulation 2007; 10(3): 262-278..
Mekhail et al, Cost Benefit of Neurostimulation for Chronic Pain, Clin f Pain Volume 20, Number 6, November/December 2004
Oswald AM, et al. Parallel processing of sensory input by bursts and isolated spikes. J Neurosci. 2004;24(18):4351-4362.
Sherman S.M. A wake-up call from the thalamus. Nature Neuroscience. 2001; 4(4):344-346
Jahnsen H, Llins R. : Voltage-dependent burst-to-tonic switching of thalamic cell activity: an in vitro study. Arch Ital Biol. 1984 Mar;122(1):73-82.
Harvey A. et al. The impact of 'bursting' thalamic impulses at a neocortical synapse. Nature Neuroscience 4, 402 - 408 (2001).
De Ridder D, et al. Burst Spinal Cord Stimulation for Limb and Back Pain. World Neurosurgery 2013. Nov;80(5):642-649.e1.
Lopez-Garcia JA et al. Membrane Properties of Physiologically Classified Rat Dorsal Horn Neurons In Vitro: Correlation with Cutaneous Sensory Afferent Input. European Journal of Neuroscience. Vol 6,
Issue 6, pages 9981007, June 1994
Squire LR, et al. Fundamental Neuroscience. 3rd Edition, Chapter 25: Somatosensory System, Academic Press (Elsevier), p. 599,2008.
Moens M, et al. Spinal cord stimulation modulates cerebral function: an fMRI study. Neuroradiology (2012) 54: 1399-1407.
Tang, R et al. Comparison of Burst and Tonic Spinal Cord Stimulation on Spinal Neural Processing in an Animal Model. Neuromodulation: Technology at the Neural Interface, 2013 n/a-n/a. doi:
10.1111/ner.12117
De Ridder D et al. Burst Spinal Cord Stimulation: Toward Paresthesia-Free Pain Suppression Neurosurgery 2010. 66:986-990.
Schu S, et al. Burst or Tonic Stimulation? First Results of a Placebo Controlled, Double-Blinded, Randomized Study for the Treatment of FBSS Patients. NANS 2013
de Vos CC., et al. Burst Spinal Cord Stimulation Evaluated in Patients With Failed Back Surgery Syndrome and Painful Diabetic Neuropathy. Neuromodulation: Technology at the Neural Interface. 2013
doi: 10.1111/ner.12116

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