Manjit S Matharu
Headache Group, Institute of Neurology & The National Hospital for Neurology and Neurosurgery
London UK
St Jude Medical
Intractable Chronic Migraine Course 22nd February 2012
ICHD-‐II Diagnostic Criteria Episodic attacks of headache lasting 4-‐72 hours with the following features:
Headache has at least two of the following characteristics:
Unilateral location
Pulsating quality
Moderate or severe pain intensity
Aggravation by routine physical activity
During headache at least one of the following:
Nausea and/or vomiting
Photophobia and phonophobia
Further sub-‐classified on basis of frequency of headaches Episodic migraine <15 days/month Chronic migraine >15 days/month
Time
Phases of Migraine
Premonitory Aura Headache & Associated Features Resolution
Complex array of symptoms reflecting focal cortical or brainstem dysfunction
Gradual evolution 5-‐30minutes (<60minutes)
Usually before headache; can be during or even
after headache
Aura symptoms occur with headache: – Always 18% – Sometimes 13% – Never 69% Types of aura: – Visual 99% – Sensory 31% – Language 18% – Motor 6%
MIGRAINE IS A FEATUREFUL HEADACHE
Pain: • Unilateral or bilateral • Throbbing, worsened by movement or activity
• Cutaneous allodynia • Neck stiffness/pain (80%)
Associated Symptoms:
Sensory hyperexcitability • Photophobia, phonophobia, osmophobia • Motion sensitivity/vertigo
Gastrointestinal disturbance • Nausea/Vomiting/Diarrhoea
ICHD-‐IIR DIAGNOSTIC CRITERIA
1. ICHD 2006 Headache Classification Committee of the International Headache Society. Olesen J et al. Cephalalgia 2006;26:742
Migraine headache occurring on of medication overuse, not attributed to another disorder.
On has at least two of the following characteristics:
Unilateral location
Pulsating quality
Moderate or severe pain intensity
Aggravation by routine physical activity
During headache at least one of the following:
Nausea and/or vomiting
Photophobia and phonophobia
and/or treated and relieved by triptan(s) or ergot before developing into a migraine
1. Stovner LJ et al. Cephalalgia 2007;27:193–210. 2. World Health Organization. The Global Burden of Disease: 2004 update, Part 3, 28–37. 3. World Health Organization. Headache disorders, 2004. 4. Natoli JL, et al. Cephalagia 2010;30:599-‐609.
One-‐year prevalence of migraine is approximately 10%1
Migraine is more prevalent than common disorders such as diabetes and asthma.2
In Europe and America, WHO estimates the prevalence of migraine to be 6–8% in men and 15–18% in women.3
Chronic migraine affects 1.4-‐2.2% of people wordwide4
Migraine 50M Chronic Migraine
7.3M
Medically Refractory Chronic Migraine
1M?
European Union
1. Menken M,Munsat T, Toole J. Archives of Neurology 2000; 57:418-420. 2. Lipton RB et al. Headache. 2001.
Migraine is one of the 20 most common causes of years of life lived with disability1
WHO global burden of disease survey rates severe migraine, along with quadriplegia, psychosis and dementia, in a group as the most disabling chronic disorders1 80% of migraine patients report severe or very severe pain2 91% of migraine patients report disability2
91% of migraine patients report disability
Lipton RB et al. Headache. 2001.
59%
67%
76%
51%
0% 20% 40% 60% 80% 100%
Missed Family/Social Leisure Activity
Household Work Productivity Reduced by 50%
Unable to Do Chores/ Household Work
Work/School Productivity Reduced by 50%
1. Natoli JL, et al. Cephalagia 2010;30:599-‐609. 2. Blumenthal AM et al Lancet 2010
71.7
56.5
67.2 61.4
44.4 48.3
0
10
20
30
40
50
60
70
80
Unable to perform normal activities
Difficult to perform normal activities
Emotional effects
Mean MSQ
score
Chronic migraine
Episodic migraine
* *
* P<0.0001
*
Affects 1.4-‐2.2% of people wordwide1
Significantly more burdensome than episodic migraine:2
Direct costs Indirect costs
Medication Absence from work (absenteeism)
Consultation Reduced productivity at work (presenteeism)
Hospital admission Lost career opportunities
Diagnostic investigations Unemployment
Migraine is an important public health problem that is associated with substantial costs1–3
In Europe, 41 million patients with migraine cost the economy €27 billion overall in 20044
1. Steiner TJ et al. Cephalalgia 2003;23:519–527. 2. Hawkins K et al. Headache 2008;48:553 563. 3. Stewart WF et al. JAMA 2003;290:2443 2454. 4. Andlin-‐Sobocki P et al. Eur J Neurol 2005;12(Suppl 1):1
Aura: Pathophysiological Hypotheses
Aura
Cortical spreading depression of Leao
Wave of excitation followed by inhibition that traverses the cortex at 3-‐6 mm/min
Wolff’s vascular hypothesis
Migraine aura secondary to cerebral hypoxia
Normal CBF
Hypo-‐ perfusion
Hyperperfusion
Hours after angiography
Headache 2 4 6 8 10 12
Wolff. Headache and other head pain. 1963 Leao. J. Neurophysiol. 1944; Leao and Morison. J. Neurophysiol. 1945 Silberstein SD et al. Headache in Clinical Practice. 2nd ed. 2002
Xenon-‐133 Studies
Normal CBF
Hypo-‐ perfusion
Hyperperfusion
Relative timing of CBF, Aura and Headache
Hours after angiography
Headache Aura
2 4 6 8 10 12
Olesen et al, Ann Neurol 1990; Olesen, Migraine and other headaches: the vascular mechanisms. 1991; Olesen, The headaches. 1993
BOLD fMRI
(i) Initial cortical gray hyperemia, with
(ii) Characteristic duration, and (iii) Characteristic velocity, which is (iv) Followed by hypoperfusion, and
shows (v) Attenuated response to visual
activation, and (vi) Recovery to baseline mean level,
and (vii) Concurrent recovery of the
stimulus driven activation (viii) Spreading phenomenon did not
cross prominent sulci
Cortical spreading depression rather than vasoconstriction is the basis of aura Hadjikhani et al, PNAS 2001
Spontaneous Episodic Migraine
Weiller et al, Nature 1995
Spontaneous Episodic Migraine
Afridi et al, Arch Neurol 2005
Chronic Migraine
Matharu et al, Brain 2004
Specific dorsal rostral pontine activation in migraine
Sphenopalatine ganglion Trigeminal
ganglion
Trigeminal nucleus
Superior salivatory nucleus
Trigeminal nerve
Meninges
Pain
Adapted from Iadecola C. Nat Med 2002; Bolay H et al. Nat Med. 2002.
Visually-‐triggered Migraine
BOLD-‐fMRI Study
BOLD signal changes in brainstem before occipital cortex signal changes (consistent with CSD) or onset of visual symptoms
Cao et al, Arch Neurol 1999; Cao et al, Neurology 2002
CSD-‐triggered Trigeminovascular Activation?
TGVS=trigemino-‐vascular system. Adapted from Pietrobon D, Striessnig J. Nat Rev Neurosci. 2003;4:386-‐398.
Vasodilation Neurogenic Inflammation
Headache Pain
Abnormal cortical activity
Hyperexcitable brain ( Ca++, Glu, Mg++)
Cortical Spreading Depression
Activation/Sensitization of TGVS
Abnormal brain stem function
Excitation of brain stem, PAG, etc.
Central Sensitization
Headache Management
Education and Support
Lifestyle modification and trigger management
Pharmacological Treatments
Psychological and behavioural
treatments
Surgical treatments
1. Kelman L. Cephalalgia 2007;27:394–402.
0
10
20
30
40
50
60
70
80
90
Stress Hormones Missed meals
Weather Sleep disturbance
Perfume /odours
Neck pain
Lights Alcohol Smoke Sleeping late
Heat Food
Percentage of p
atients
Triggers
• A high percentage of migraine patients report triggers • 76% to 95% of patients report triggers1 • The mean number of triggers per patient is 6.71
Headache Management
Education and Support
Lifestyle modification and trigger management
Pharmacological Treatments
Psychological and behavioural
treatments
Surgical treatments
Acute medications are used to provide relief of pain and associated symptoms1
Overuse of acute medication is common in individuals with chronic migraine1–3
20-‐30% in population; 50%–80% in headache clinics Avoid opioids and ergots if possible in patients with frequent attacks4,6 Limit the use of acute medication to <3 days/week4,5
Non-‐specific Treatments Specific Treatments
• Paracetamol 1g • NSAIDs (high-‐dose & soluble):
Aspirin 600-‐900mgs Ibuprofen 600-‐800mgs Naproxen 500-‐1000mgs Tolfenamic acid 200mgs Diclofenac 50-‐75mgs
• Opioids • Use concurrently with Prokinetics:
Domperidone 10-‐20mgs Metoclopramide 10mgs
• Triptans: Sumatriptan Rizatriptan Zolmitriptan Almotriptan Eletriptan Naratriptan Frovatriptan
• Ergot derivatives: Ergotamine 1-‐2mg tablet or suppository
1. Silberstein SD et al. eds. Headache in Clinical Practice. 2nd ed. London: Martin Dunitz; 2002:69–146. 2. Lipton RB et al. Neurology 2003;61;154–155. 3. Wang SJ et al. Pain 2001;89:285–292. 4. Diener HC et al. Lancet Neurol 2004;3:475–483. 5. Silberstein SD et al. eds. Headache in Clinical Practice. 2nd ed. London: Martin Dunitz; 2002:69–111. 6. Bigal ME et al. Headache 2008;48:1157–1168
Develops through chronic overuse of acute medication taken to treat headache or other pain1
Defined in the 2006 ICHD-‐IIR guideline as:2 – Headache on – Regular overuse for >3 months of acute symptomatic treatment drugs, during which time headaches have developed or worsened markedly
Overuse of all headache medication taken on an ad hoc basis to relieve pain may result in medication overuse headache3
Most commonly associated with regular use of: – Simple analgesics or NSAIDs on – Opioids, ergots, combination analgesics or triptans on 3
Preventives less effective with concurrent medication (analgesic) overuse
1. Manack A et al. Headache 2009;49:1206 2. ICHD 2006 Headache Classification Committee of the International Headache Society. Olesen J et al. Cephalalgia 2006;26:742 3. World Health Organization (WHO) in collaboration with the European Headache Federation (EHF). J Headache Pain 2007;8:S1 .
Very common Worldwide prevalence estimated to be 2%
60–85% patients seen in tertiary referral centres with chronic daily headache have medication overuse headache Greater impact on daily functioning than episodic migraine In one study significant impairment or reduction in function in 71% of days
1. Diener HC, Limmroth V. Lancet Neurol 2004;3:475–483. 2. Katsarava Z et al. Curr Neurol Neurosci Rep 2009;9:115–119.
* 15 days/month: simple analgesics, combinations of drugs; or 10 days/month: combination analgesics, ergotamines, triptans, opioids, barbiturates.
Preventative therapy
FAIL
Medication overuse1,2*
Detoxification
Out-‐patient Setting Day Case or In-‐patient Setting
• Beta-‐blockers – Propranolol
• Antidepressants – Amitriptylline
• Serotonergic antagonist Pizotifen Methysergide
• Antiepileptic drugs (AEDs) Topiramate Valproate Gabapentin
• Calcium channel antagonists – Flunarizine
• Botox • ACE inhibitors and ARBs
– Lisinopril – Telmisartan
• Herbs, Vitamins and Minerals
• Botox • Greater occipital nerve blocks • Intravenous dihydroergotamine infusions
Headache Management
Education and Support
Lifestyle modification and trigger management
Pharmacological Treatments
Psychological and behavioural
treatments
Surgical treatments
Chronic Migraine is a relatively common primary headache disorder Migraine is a neurovascular disorder Chronic Migraine is a very painful and highly disabling disorder
While there are numerous medical treatment options, a subset of these patients is intractable to conventional medical treatments. There is a clear need for novel approaches for the management of this highly disabled patient group
• Headache on > 15 days/month for at least 3 months • Affects 3-‐4% of the population • Descriptive term • Not diagnosis • Encompasses heterogeneous group of primary and secondary headache syndromes
DEFINITION
1. Silberstein SD et al. Neurology 1996;47:871
After secondary causes are ruled out
Primary headache disorders
Chronic daily headache Frequency
Chronic migraine Chronic tension-‐ type headache
New daily persistent headache
Hemicrania continua
Episodic headache Frequency <15 days/month
Short-‐duration chronic daily headache
Duration <4 hours or multiple discrete episodes
With or without medication overuse
Long-‐duration chronic daily headache
Daily or near-‐daily headache lasting
CAUSES
Migraine is typically most prevalent during the most productive years of adulthood – between the ages of 20 and 50 years1 One study suggests that 75–90% of the total economic cost of migraine is associated with absenteeism or reduced/lost workplace productivity2
People with chronic migraine are less likely to be actively working full-‐time, with an employment rate that is 81% of that for patients with low-‐frequency headache3
For those patients with chronic migraine who can work, their disorder results in a >50% reduction in productivity at work or school4
1. Stovner LJ et al. Eur J Neurol 2006;13:333–345. 2. Brown JS et al. Headache 2005;45:1012 3. Stewart WF et al. Poster presented at the 14th International Headache Congress, September 10–13 2009, Philadelphia, PA, USA. 4. Munakata J et al. Headache 2009;49:498–508.
Primary diagnosis ICHD-‐II migraine or chronic migraine
Refractory Headaches cause signi quality of life despite modi factors, and adequate trials of acute and preventive medicines with established ef 1. Failed adequate trials of preventive medicines, alone or in combination, from at least 2 of 4 drug classes:
a. Beta-‐blockers b. Anticonvulsants c. Tricyclics d. Calcium channel blockers
2. Failed adequate trials of abortive medicines from the following classes, unless contraindicated:
a. Both a triptan and DHE intranasal or injectable formulation b. Either NSAID or combination analgesics
Disabling With signi disability
Schulman et al, Headache 2008;48:778-78
Manjit S Matharu Headache Group, Institute of Neurology &
The National Hospital for Neurology and Neurosurgery London
UK
St Jude Medical Intractable Chronic Migraine Course
22nd February 2012
Weiner 1995 Started performing ONS in patients who responded to repeated greater occipital nerve blocks
Weiner & Reed, 1999 Peripheral neurostimulation for control of intractable occipital neuralgia Most of these patients were reported to had chronic migraine in subsequent functional imaging study Subsequently, numerous groups reported positive experiences in several primary and secondary headache syndromes
Weiner R, Reed KL. Neuromodulation. 1999;2(3):217-21.
PRIMARY HEADACHES
Chronic migraine Chronic cluster headache Hemicrania continua
SUNCT
SECONDARY HEADACHES
Occipital neuralgia Cervicogenic headache Post-‐traumatic headache
• Open Label series • ONSTIM Study • PRISM Study • St Jude Medical Study
OPEN LABEL CASE SERIES
Author Number Mean duration of disorder
(yrs)
Number improved (>50%)
Follow up (yrs)
Popeney 25 10 22 1.5
Oh 10 12 10 0.5
Matharu 8 5.8 8 1.5
Schwedt 8 Not stated 3 1.5
TOTAL 51 43 (84%)
Popeney& Alo Headache 2003; Oh et al. Neuromodulation 2004; Schwedt et al Cephalalgia 2007; Matharu et al Brain 2004
Medication overuse probably negatively affects outcome
Occipital Nerve Stimulation for the Treatment of Intractable Chronic Migraine Headache
Saper JR, et al Cephalalgia. 2011;31(3):271-285.
Multicentre, prospective, single blind, controlled feasibility study 66 medically intractable chronic migraine Failed at least 2 classes of preventives Bilateral ONS Randomised 2:1:1 to
– Adjustable stimulation (AS) – Preset stimulation (PS) – Medical Management (MM)
• Responder defined as: – 50% reduction in headaches days/month – 3-‐point drop (VRS 0-‐10) in pain intensity
Patients enrolled
who responded to an occipital nerve block Preset Stimulation (PS)
Medical Management (MM)
2:1:1 ratio
Adjustable Stimulation (AS)
12 Weeks
(Active, N=29 completed)
(Control, N=16 completed)
(Comparator, N=17 completed)
This prospective, randomized, double-blind, controlled study examined the efficacy and safety of occipital nerve stimulation in adult chronic migraine patients.
6.7
1.5 1
0
1
2
3
4
5
6
7
8
Adjustable Stimulation (AS)
Preset Stimulation (PS)
Medical Management
(MM)
27.0%
8.8%
4.4%
0%
5%
10%
15%
20%
25%
30%
Adjustable Stimulation (AS)
Preset Stimulation (PS)
Medical Management
(MM)
Mean percent reduction (SD) in headache days per month
Mean (SD) reductions in actual headache days per month
(44.8)
(28.6)
(19.1)
(10.0)
(4.6)
(4.2)
Baseline 22.4+6.3 23.4+5.1 23.7+4.3
Reduction (SD) in overall pain intensity
Responder rates
39%
6% 0%
0%
10%
20%
30%
40%
50%
Adjustable Stimulation (AS)
Preset Stimulation (PS)
Medical Management
(MM)
0
0.5
1
1.5
2
Adjustable Stimulation (AS)
Preset Stimulation (PS)
Medical Management
(MM)
1.6
0.6 0.5
Adverse Events %
Lead migration/dislodgement 24%
Therapeutic product ineffective 16%
Implant site (lead/extension tract) infection 14%
Incision site complications 8%
Implant site (IPG) infection 4%
Implant site (IPG) pain 4%
Neck pain 4%
Burning sensation 2%
Discomfort 2%
Extension migration/dislodgement 2%
High impedance 2%
Hypotension 2%
Adverse Events %
Implant site (IPG) hematoma 2%
Implant site (IPG) irritation 2%
Implant site (lead/extension tract) inflammation 2%
Lead fracture 2%
Migraine 2%
Post-procedural nausea 2%
Post-procedural pain 2%
Rash 2%
Sensation of pressure 2%
Stitch abscess 2%
Suture-related complications 2%
Tenderness 2%
Fifty-six device-related adverse events occurred in 36 out of 51 patients.
Multicentre, prospective, double blind, controlled study 132 migraine patients ( 6 days/month, 4 hrs each) Failed at least 2 acute and 2 preventive treatments Bilateral ONS Trial stimulation for 5-‐10 days Randomised in 1:1 ratio for 12 weeks
– Active stimulation (<12.7mA, 60 Hz, 250 sec) – Sham stimulation (>1mA, 2Hz, 10 sec for 1sec/90 mins)
• All subjects has active stimulation from 12 weeks onwards • Primary end-‐point: change in headache days/month at 12 weeks
Lipton RB, et al. PRISM study: Occipital nerve stimulation for treatment-refractory migraine. Presented at: 14th Congress of the International Headache Society; September 10-13, 2009; Philadelphia, PA.
Patients enrolled
1:1 ratio
Active Stimulation
12 Weeks
This prospective, randomized, double-blind, controlled study examined the safety and efficacy of occipital nerve stimulation for the preventive treatment of refractory migraine in 132 patients in 13 centres.
5–10 days
Sham Stimulation (Control)
Trial stimulation to assess its predictive
value
Two-year follow-up conducted to assess
safety.
Mean reduction (SD) in migraine days per month
Mean percent reduction in migraine days per month
Primary efficacy measure: reduction in migraine days per month
5.5
3.9
0
1
2
3
4
5
6
Active Stimulation Sham Stimulation
(8.7)
(8.2)
27% 20%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
Active Stimulation Sham Stimulation
Adverse Events Number of Cases
Non-‐targeted area sensory symptoms 18.0%
Implant site pain/discomfort 17.3%
Infection 15.0%
Incision site pain/discomfort 7.9%
Lead migration 6.8%
A two-year follow-up was conducted to assess safety. Complications included the following:
In this study, occipital nerve stimulation did not produce a statistically significant benefit in the active vs. control group. However, subgroup analysis identified several predictors of a favourable response to stimulation, including the following:
Not overusing headache medications Not using opiates A positive response to a trial stimulation
Silberstein et al. The Safety and Efficacy of Occipital Nerve Stimulation for the Management of Chronic Migraine. Presented at: 15th Congress of the International Headache Society; June 23-‐26, 2011; Berlin.
Multicentre, prospective, double blind, controlled study 157 chronic migraine patients, with VAS score > 6/10 Headache pain is posterior head pain or pain originating in the cervical region Failed at least 2 acute and 2 preventive treatments Bilateral ONS Randomised in 2:1 ratio for 12 weeks
• All subjects has active stimulation from 12 weeks onwards • Primary end-‐point: 50% VAS with no increase in average headache frequency or duration.
• Secondary end-‐points: MIDAS-‐disability days, Headache Index, Zung Pain and Distress Scale, Patient Satisfaction, Safety
Patient Enrolled
PNS Implanted
Randomize and Device Activation
Group A: Active
Group B: Control (Blind)
2:1 Ratio
52-‐week visit 24-‐week visit 12-‐week visit 4-‐week visit 80-‐ to 90-‐day roll in
Control pts were blinded using pt programmers that did not communicate with the IPG, plus pts were also told that a range of settings were being tested. Neither the patient nor the study investigator knew whether the patient was active or
control (“double-blind”) during the first 12 weeks.
Primary Outcome 50% VAS reduction with no increase in average headache frequency or duration
0 2 4 6 8
10 12 14 16 18
Active Sham
P=0.21
1 Two-sided test of no difference 2 One-sided lower 95% confidence bound
Continuous Proportion Responder Analysis Based on Mean Daily Average Pain Intensity VAS Measurements With No Increase in Average Headache Frequency or Duration
Significance demonstrated at 30% reduction in pain (p-value=0.011)
% reduction from baseline
Control Group % responders
(n=52)
Active Group % responders
(n=105) p-‐value1
met protocol objective (>10% dif.)2
0,0% 38,5% 69,5% <0,001 Yes
10,0% 30,8% 58,1% 0,001 Yes
20,0% 19,2% 41,9% 0,005 Yes
30,0% 17,3% 37,1% 0,011 Yes
40,0% 15,4% 25,7% 0,143 No
50,0% 13,5% 17,1% 0,553 No
60,0% 9,6% 11,4% 0,731 No
70,0% 1,9% 4,8% 0,664 No
80,0% 1,9% 3,8% 1 No
90,0% 0,0% 1,0% 1 No
100,0%
0%
20%
40%
60%
80%
100%
0% 20% 40% 60% 80% 100%
Percen
tage of P
atients
Percentage of Pain Reduction
Patients Achieving Various Levels of Pain Relief
Control (n=52) Active (n=105)
Visit Control Group (n=52) Active Group (n=105) P-Value
Baseline
Mean (± std) 17,1 (± 8.2) 20,5 (± 7,6) 0,011
Week 12
Mean Change1 -4,3 (25,1%) -7,3 (35,6%) 0,02
Difference (95% CI) -3,0 (-5,5, -0,5)
Mean Baseline and Change From Baseline in Headache Days per month—Last Value Carried Forward
Patient diaries recorded whether or not patients had a headache each day, the daily average headache intensity, and the daily headache duration, in hours. Data was used to identify Headache Days, defined as a day with a headache
lasting four or more hours with at least moderate intensity.
1 Adjusted for study center, prior use of alternative therapy, and baseline
Significant reduction -3.0 days in Headache Days (per month) between Active & Control groups (p=0.02)
Visit Control Group (n=51) Active Group (n=99) P-Value
Baseline
Mean (± std) 56,0 (± 17,2) 59,5 (± 16,2) 0,221
Week 12
Mean Change1 -6,1 -13,6 0,006
Difference (95% CI) -7,5 (-12,8, -2,2)
Mean Baseline and Change From Baseline in Daily Average Pain Intensity VAS Measurements By Visit —Last Value Carried Forward
The patient-recorded average pain intensity in their electronic diary using a VAS with a 100 mm line to indicate severity progression.
Patients were asked to record these measurements on each day that they experienced headache.
1 Adjusted for study center, prior use of alternative therapy, and baseline
The active group had significant reduction in relief in average pain intensity on days with pain vs. the control group (P=0.006).
Visit Control Group (n=52) Active Group (n=105) P-Value
Baseline
Mean (± std) 152,7 (± 77,1) 158,4 (± 76,8) 0,664
Week 12
Mean Change1 -20,4 -64,6 <0,001
Difference (95% CI) -44,1 (-65,4, -22,9)
Mean Baseline and Change From Baseline in the MIDAS Headache Questionnaire Sum of Items 1 – 5—Last Value Carried Forward
The Migraine Disability Assessment (MIDAS) is a questionnaire which measures headache-related disability during the previous 90 days based on five disability questions.
1 Adjusted for study center, prior use of alternative therapy, and baseline
The MIDAS questionnaire was completed at baseline and 12 weeks after the system was implanted. The reduction in disability of 44.1 days between the groups is statistically significant (p<0.001).
The differences reported between the Active and Control Groups for both measures were statistically significant (p<0,001).
17,2%
42,1%
0%
20%
40%
60%
80%
100%
Percentage of Pain Relief Since Surgery
Control Group (n=52) Active Group (n=105)
19,2%
51,4%
0%
20%
40%
60%
80%
100%
Percentage of Patients Satisfied With Headache Relief
Control Group (n=52) Active Group (n=105)
Active group participants reported (on average) 42,1% pain relief and 51,4% of them were satisfied with their level of pain relief.
Adverse Event + Total
(N=153) n (%)
Lack of efficacy/return of symptoms 15 (9,8%)
Persistent pain and/or numbness at IPG/lead site 15 (9,8%)
Normal battery depletion 12 (7,8%)
Unintended stimulation effects 10 (6,5%)
Lead migration 9 (5,9%)
Battery failure 8 (5,2%)
Lead breakage/fracture 5 (3,3%)
Infection 4 (2,6%)
Battery passivation 3 (2,0%)
Device malfunction–programmer 3 (2,0%)
A total of 76 patients experienced one or more anticipated adverse events during the first open label study phase (50 in the Active group and 26 in the Control group).
A total of 114 adverse events occurred in these 78 patients. All events were reviewed and classified into the appropriate category. According to this classification, 42 events were classified as hardware-related, 28 events were classified as biological-related, 28 events were classified as stimulation-related, and 16 events were classified as non-device/procedure-related.
Adverse Event + Total
(N=153) n (%)
Nausea/vomiting 3 (2,0%)
Expected post-‐op pain/numbness at IPG/lead site 2 (1,3%)
Skin erosion 2 (1,3%)
Hematoma 1 (0,7%)
Seroma 1 (0,7%)
Wound site complications 1 (0,7%)
Pain or swelling at IPG site–trauma-‐related 1 (0,7%)
Allergic reaction to surgical materials 1 (0,7%)
Device malfunction–IPG 1 (0,7%)
IPG migration 1 (0,7%)
Anatomical Convergence of Trigeminal and Cervical input
MECHANISM OF ACTION
Functional Convergence of Trigeminal and Cervical input
Bartsch et al, Brain 2002
MECHANISM OF ACTION
1. Effect at Segmental level
Gate-Control Theory of Pain Activation of somatosensory afferent A- nerve fibres blocks nociceptive transmission at a segmental level
2. Involvement of Supraspinal
Structures
Gate control at supraspinal level Activation of descending antinociceptive pathways
3. Neuroplasticity
MECHANISM OF ACTION
Paraesthesia-related rCBF changes
Significant activation in the dorsal rostral pons, anterior cingulate cortex and left pulvinar
Matharu et al, Brain 2004
MECHANISM OF ACTION
Patients with chronic migraine are often left without effective treatment, leading lives that are painful and compromised.1
Occipital nerve stimulation involves a minimally invasive surgical procedure.
While the body of evidence is still emerging, ONS appears to be promising in managing the pain and disability of intractable chronic migraine.
Frequent causes of adverse events are related to lead migration.
Predictors of response and long-‐term outcome are largely unknown
Reserved for medically-‐intractable and highly disabled patients
Performed in experienced headache centres
1. Saper JR, Dodick DW, Silberstein SD, McCarville S, Sun M, Goadsby PJ; ONSTIM Investigators. Occipital nerve stimulation for the treatment of intractable chronic migraine headache: ONSTIM feasibility study. Cephalalgia. 2011;31(3):271-285.
Category Adverse Event + Total
(N=153) n (%)
Patients with one or more anticipated AE 76
Hardware-‐Related
Normal battery depletion 12 (7,8%)
Lead migration 9 (5,9%)
Battery failure 8 (5,2%)
Lead breakage/fracture 5 (3,3%)
Battery passivation 3 (2,0%)
Device malfunction–programmer 3 (2,0%)
Device malfunction–IPG 1 (0,7%)
IPG migration 1 (0,7%)
Stimulation-‐Related
Lack of efficacy/return of symptoms 15 (9,8%)
Unintended stimulation effects 10 (6,5%)
Nausea/vomiting 3 (2,0%)
A total of 76 patients experienced one or more anticipated adverse events during the first open label study phase (50 in the Active group and 26 in the Control group).
A total of 114 adverse events occurred in these 78 patients. All events were reviewed and classified into the appropriate category. According to this classification, 42 events were classified as hardware-related, 28 events were classified as biological-related, 28 events were classified as stimulation-related, and 16 events were classified as non-device/procedure-related.
Category Adverse Event + Total
(N=153) n (%)
Patients with one or more anticipated AE 76
Biological
Persistent pain and/or numbness at IPG/lead site 15 (9,8%)
Infection 4 (2,6%)
Expected post-‐op pain/numbness at IPG/lead site 2 (1,3%)
Skin erosion 2 (1,3%)
Hematoma 1 (0,7%)
Seroma 1 (0,7%)
Wound site complications 1 (0,7%)
Pain or swelling at IPG site–trauma-‐related 1 (0,7%)
Allergic reaction to surgical materials (sutures, antibiotic, anesthesia) 1 (0,7%)
Non-‐Device-‐Related Other 16 (10,5%)
A total of 76 patients experienced one or more anticipated adverse events during the first open label study phase (50 in the Active group and 26 in the Control group).
A total of 114 adverse events occurred in these 78 patients. All events were reviewed and classified into the appropriate category. According to this classification, 42 events were classified as hardware-related, 28 events were classified as biological-related, 28 events were classified as stimulation-related, and 16 events were classified as non-device/procedure-related.
65
Patient selection for successful therapy Zaza Katsarava
Headaches
Headache = 80% Migraine = 15-18% TTH = 30-70% Chronic headache 3-4%
Chronic Headache
Chronic Headache = HA
The reasons to define chronic vs. episodic HA Individual burden Burden of social environment Co-morbidities Costs
Chronic Headache
The prevalence of chronic headache is about 3-4% For systemic review see Stovner et al, 2006
69
After Secondary Causes Are Ruled
Out
Episodic Headache Frequency <15
days/month
Short-Duration Chronic Daily
Headache Duration <4 hours or
multiple discrete episodes
Chronic Daily Headache (Long
Duration) Daily or near-‐daily
headache lasting
Chronic Tension-
Type Headache
New Daily Persistent Headache
Hemicrania Continua
Silberstein SD et al. Neurology. 1996;47:871-‐875. Dodick D. N Engl J Med. 2006;354:158-‐165.
With or Without Medication
Overuse
Chronic Headache Frequency
days/month
Primary Headache Disorders
Chronic Migraine
70
CM = migraine on 15 days/month CTTH = TTH on 15 days/month
71
Visu
al a
nalo
gue
scal
e
Visu
al a
nalo
gue
scal
e
72
Visu
al a
nalo
gue
scal
e
Visu
al a
nalo
gue
scal
e
73 Vi
sual
ana
logu
e sc
ale
time
With migraine features
Without migraine features
With migraine features
Without migraine fetures
Triptan
Migraine
TTH? Abortive Migraine? TTH
Abortive Migraine
74
IHS 2004, CM = migraine on 15 days/month No medication overuse Diary is needed Rely on patients recall Too restrictive
75
IHS 2006, CM =
Migraine HA on 8 HA days is migraine No medication overuse
76
Allergan, PREEMPT, CM =
Migraine HA on 50% is migraine
77
American way to do it, Silberstein-‐Lipton CM =
Migraine HA on
No diary is needed
78
Mail/phone interviews
Population-based sample N = 18,000
9968 respondents Response rate = 63.4%
Annual follow-ups
79
1. Katsarava et al. Cephalalgia, 2011. 2. Olesen J et al. Cephalalgia.
2006;26(6):742-746. 3. Silberstein SD et al. Headache.
1994;34:1-7.
Chronic Migraine definition IHS, 2006 ( migrainous) ICHD-2 definition2
Chronic Migraine definition S-L ( migrainous) Silberstein-Lipton Criteria3
2.8%
Chronic Migraine definition PREEMPT ( migrainous)
1.9% 0.5%
0.4%
Chronic Daily Headache (
CM according to S-L = 185
IHS MIG criteria
TTH criteria
IHS CM = 45
The rest, 185 – 45 = 140
IHS TTH = 40
What is the rest? N = 100
81
CM is NOT just more MIG
82
Definition Females Age BMI Low
Education Medication Overuse*
CM-‐I ( 70% 44 26.4 70% 27%
CM-‐II (migrainous, including overuse) 69% 45 26.5 73% 31%
CM-‐III ( any migrainous) 71% 46 25.9 78% 11%
High-‐frequency EM (9-‐14 days/month) 70% 40 24.3 66% 13%
Low frequency EM (0-‐8 days/month) 66% 40 24.1 60% 16%
Katsarava et al. Migraine Trust 2008. Abstract. GHC = German Headache Consortium.
83
41
31 3026
1519
0
10
20
30
40
50
60
70
Allergies or Hay Fever
Sinusitis Asthma Bronchitis Depression Chronic Pain
Anxiety High Blood Pressure
High Cholesterol
Obesity Arthritis
Chronic migraineEpisodic migraine
Buse D et al. J Neurol Neurosurg Psychiatry. 2010; In press.
%
*p<0.05.
Data from the American Migraine Prevalence and Prevention (AMPP) study.
*
*
* *
* *
*
* * *
*
• Chronic migraine was defined as reported ICHD-2 diagnosis of migraine and days/month
9944 responders (of 18.000 = 55%) Prevalences:
HA : cHA = 255, eHA = 5361, noHA = 4040, missing = 288 MIG : cMIG = 108, eMIG = 1601, noHA = 4030, 4205 excluded TTH : cTTH = 50, eTTH = 1203, noHA = 4030, 5283 excluded Combination of MIG and TTH and unclassifiable excluded Chronic back pain = 1290
84
85
N cBP OR 95% CI
No HA 3259 316 (9.6%) Referent = 1
Episodic HA 4903 807 (16.5%) 2.3 2.0 – 2.7
Chronic HA 229 146 (63.7%) 14.5 10.7 – 20.0
Age (in years) 1.03 1.02 – 1.04
Males 3925 489 (12.5%) Referent = 1
Females 4466 801 (17.9%) 1.4 1.2 – 1.6
No daily drinking 7437 1125 (15.1%) Referent = 1
Daily drinking 954 143 (15.0%) 1.1 0.9 – 1.4
No smoking 5850 808 (13.8%) Referent = 1
Smoking 2541 466 (18.3%) 1.4 1.2 – 1.6
High education 2879 279 (9.7%) Referent = 1
Low education 5512 981 (17.8%) 1.6 1.3 – 1.8
BMI 4667 602 (12.9%) Referent = 1
BMI 25-‐30 2717 417 (15.3%) 1.1 1.0 – 1.3
BMI 1007 239 (23.7%) 1.8 1.5 – 2.1
86
N cBP OR 95% CI
No Headache 3238 314 (9.7%) Referent = 1
Episodic MIG 1462 279 (19.1%) 2.6 2.1 – 3.2
Chronic MIG 100 66 (66%) 15.8 10.2 – 24.5
Age (in years) 1.03 1.02 – 1.04
Males 2410 250 (10.4%) Referent = 1
Females 2390 409 (17.1%) 1.4 1.1 – 1.7
No daily drinking 4192 580 (13.8%) Referent = 1
Daily driking 608 67 (11.0%) 0.97 0.7 – 1.3
No smoking 3329 408 (12.3%) Referent = 1
Smoking 1471 243 (16.5%) 1.5 1.2 – 1.8
High education 1473 122 (8.3%) Referent = 1
Low education 3327 520 (15.6%) 1.6 1.3 – 2.0
BMI 2556 304 (11.9%) Referent = 1
BMI 25-‐30 1622 214 (13.2%) 1.1 0.9 – 1.3
BMI 622 124 (19.9%) 1.6 1.2 – 2.0
87
N cBP OR 95% CI
No Headache 3238 314 (9.7%) Referent = 1
Episodic TTH 1104 170 (15.4%) 2.1 1.7 – 2.7
Chronic TTH 47 29 (61.7%) 13.7 7.4 – 25.3
Age (in years) 1.03 1.02 – 1.04
Males 2435 247 (10.1%) Referent = 1
Females 1954 266 (13.6%) 1.4 1.1 – 1.7
No daily drinking 3771 424 (11.2%) Referent = 1
Daily driking 618 79 (12.8%) 1.2 0.9 – 1.6
No smoking 3094 330 (10.7%) Referent = 1
Smoking 1295 176 (13.6%) 1.4 1.1 – 1.7
High education 5890 104 (17.7%) Referent = 1
Low education 3013 397 (13.2%) 1.5 1.2 – 1.9
BMI 4923 207 (4.2%) Referent = 1
BMI 25-‐30 2857 188 (6.6%) 1.3 1.02 – 1.6
BMI 1067 102 (9.6%) 2.0 1.5 – 2.6
Central sensitization Blink reflex and pain evoked potentials in MOH Transient increase, normalizing again after withdrawal (Ayzenberg et al. 2006)
101520253035404550
Controls
Ep migraine
Triptan MOH
Analgesic MOH
Triptan MOH
Analgesics MOH
3. Release of pain-enhancing neuropeptides, such as CGRP
5. Activation of cortical pain centers via thalamus
Thalamus
4. Activation of trigeminal nucleus caudalis can result in central sensitization
Spinothalamic track
Trigeminal Nerve
Trigeminal Gangli
on
TNC
2. Stimulation of meningeal sensory nerve (trigeminal)
Vessel dilation
Nerve
Peptide release
Inflammation
6. PAIN
CGRP = calcitonin gene-related peptide; TNC = trigeminal nucleus candalis.
1. Pietrobon D et al. Nat Rev Neurosci. 2003;4:386-398.
2. Pietrobon D. Neuroscientist. 2005;11:373-386.
1. Central disinhibition
Post-traumatischer Kopfschmerz Reversible VBM changes in chronic posttraumatic headache
Transformation is often gradual and can evolve over several months or years1,2
Transformation is neither inexorable nor irreversible; spontaneous or induced remissions are possible and common1,2
Transformation happens in some but not all episodic patients (~3% of episodic migraine sufferers)2
91
1. Lipton RB. Neurology. 2009;72:S3-S7. 2. Bigal ME, Lipton RB. Curr Opin Neurology
2008;21:301-308.
No migraine
Low-frequency episodic migraine
High-frequency episodic migraine
Chronic migraine
Right diagnosis Multimodal approach
Patient education Psychological co-morbidities Physiotherapy
Stop medication overuse (if any) Preventive medication
Topiramate, BOTOX Betablockers, Valproate etc.
Right diagnosis
Do not miss secondary headache Do not mix CM and CTTH Do not miss MOH Do consider psychiatric co-morbidities
??? Medication overuse headache
Chronic headache with medication overuse
Suggestion for IHS classification
17. Chronic migraine due to ..... 17.1. divorce 17.2. hyperactive child 17.3. sick and bed fasted parent 17.4. ………….
1. Diener HC, Limmroth V. Lancet Neurol. 2004;3:475-483. 2. Katsarava Z et al. Curr Neurol Neurosci Rep. 2009, 9:115-119.
Medication Overuse1,2
Preventive Therapy Detoxification
* 15 days/month: simple analgesics, combinations of drugs; or 10 days/month: combination analgesics, ergotamines, triptans, opioids, barbiturates.
Education Withdrawal Preventive medication Psychological treatment Follow up
4
Diener HC, Limmroth V. Lancet Neurol. 2004;3:475-483.
Single analgesic Combination analgesics
Ergotamines Triptans
Days of Withdrawal Therapy
0 1 3 4 5 6 7 8 9 10 11 12 2 13 14
100 90 80 70 60 50 40 30 20 10
Patie
nts
With
Hea
dach
e (%
) 3
2
1
0
Hea
dach
e In
tens
ity
Days of Withdrawal Therapy 1 3 5 6 7 8 9 10 11 12 2 13 14
Hagen K et al. Cephalalgia. 2009;29:221-232.
Controls Abrupt withdrawal only Prophylaxis from the start
Months Following Withdrawal
No.
of H
eada
che
Day
s/M
onth
30
25
20
15
10
5
0 0 2 3 4 5 6 7 8 9 10 11 12 1
Prophylaxis from the start
Controls Abrupt withdrawal only
Month 3 Month 5 Month 12 0
10
60
50
40
30
20 Pa
tient
s Ex
hibi
ting
a 50
% R
educ
tion
in
Hea
dach
e D
ays/
Mon
th
(%)
P = 0.01
Months Following Withdrawal
1. Everything that is true for conservative treatment is also true for ONS
1. Education 2. Realistic goals 3. Take your time 4. Give time to patients
Conservative treatment
1. Betablocker (Metoprolol 100-200mg) 2. Calcium channel antagonist (Flunarizine 5-10mg) 3. Valproic acid 600-900mg 4. Topiramate 50-200mg 5. BOTOX
Topiramate Efficacy Mean Change in Headache Days 0.7
0.20.1
-0.6
0.5
-3.5*
-5.4**-4.7**
-2.9-3.0*
-6-5-4-3-2-1012
Wk 4 Wk 8 Wk 12 Wk 16 Last 4 wks
Placebo TopiramatePrimary endpoint
* p < 0.05 vs placebo ** p < 0.01 vs placebo
26 25 20 15 27 32 30 25 24 32
Patients
BOTOX Efficacy Mean Change in Headache Days
Peripheral Nerve Stimulation for the Management of Intractable Chronic Migraine Implant Techniques
Laurence Watkins Consultant Neurosurgeon National Hospital for Neurology & Neurosurgery, London
Intractable Chronic Migraine Course, Leiden February 2012
Introducing a novel procedure
Theoretical background and peer support Registered with NICE (on hold until CE mark awarded)
Likely to now “re-‐visit” guidance Business case to Trust – novel procedures protocol Support from Trust management, R&D, host PCT (Funding Body) Cadaveric workshops Developing a PCT “application pack” and a strict protocol for
Multidisciplinary assessment Rigorous consent procedure so that patients are aware of relative novelty of the procedure Documented audit of complications and outcome
First Meeting (with implanter)
Check have been fully assessed in Headache Neurology Clinic (chronic, disabling, intractable) General fitness & airway satisfactory; reflux? MRI ? (because can’t have MRI once ONS is implanted) Any major surgery planned ? (because restriction of monopolar diathermy once ONS implanted) Explaining procedure
Discussion with patient
Known risks: may not help infection requiring removal of implant electrode migration neck stiffness breakage or failure of components tethering to skin or muscle skin erosion
Clearance from Funding Body/PCT
Hospital Stay
Typically 3-‐4 days, but could be reduced if pre-‐op assessment, implant activation and patient education all done in clinic Postoperative programming of the implant Teaching patient to use the “handset control” +/-‐ recharger
Follow up clinics
Typically 4 in first year Joint assessment with Headache Neurologist and Specialist Nurse, additional post-‐operative appointments in Neurosurgery Clinic. Sometimes all combined in day care unit Gradually refine the settings to get best response (headache diary), without patient discomfort
Stages of the operation
Insertion of electrodes LA + Sedation
Test stimulation of electrodes Awake
Insertion of battery and tunnelling of leads Asleep (GA with LMA)
Alternatively GA throughout if difficult airway or reflux (or patient preference)
USA: 2 stage procedure
Occipital Nerve Anatomy PNS electrode should overlay the course of the occipital nerves Epifascial plane Direction of insertion
Medial to lateral Lateral to medial
Fluoroscopic control Anchoring
Lead Placement (Anchor Midline)
Occipital Nerve Anatomy PNS electrode should overlay the course of the occipital nerves Epifascial plane Direction of insertion
Medial to lateral Lateral to medial
Fluoroscopic control Anchoring
Main technical challenges
Placing electrodes to get paraesthesiae Anchoring/looping the electrodes Minimising infection risk Not “instant” result so can’t really do “trial electrodes”
Technique first described for Occipital Neuralgia
Then for Transformed (Chronic) Migraine
Lead Placement (Anchor at Mastoid)
Procedural Details
Procedural Details
Procedural Details
Anchoring the Electrodes
Attach to the hard underlying fascia Use non-‐absorbable sutures Choice of anchor
long (tubular) anchor, butterfly anchor others commercially available
Anchor direction—no kinks Loops at “every level” (cervical, chest and behind IPG)
Lead Tunneling and IPG Placement: Gluteal, Infraclavicular, or Abdominal
CAUTION: It is important to place strain relief loops at the site of the lead-extension connection and at the IPG connection.
Migraine Study Key Adverse Events Summary
Adverse Event Controlled Phase Open-Label Phase
Persistent pain, numbness at implant site 23 (15%) 15 (10%)
Lead migration 20 (13%) 9 (6%)
Unintended stimulation effects (migration?) 7 (4%) 10 (7%)
Infection 7 (4%) 4 (3%)
Skin erosion 6 (4%) 2 (1%)
Lead breakage, fracture 2 (1%) 5 (3%)
“Out” Migration
Migration of occipital nerve stimulation electrode leads Both left and right leads have migrated away from their original position Try reprogramming prior to revision surgery
Extreme “Out” Migration
“Extreme” migration of occipital nerve stimulation electrode lead The electrode lead has migrated all the way toward the generator pocket
“In” Migration
“In” migration of the occipital nerve stimulation electrode lead. A. Original electrode lead position, B. Electrode position 8 month after insertion
with “in” migration to the contralateral side of the neck
A. B.
Insertion Plane Too Deep Too Superficial
Skin Erosion
PRECAUTION: Skin Erosion—Because PNS leads used to aid in the management of intractable chronic migraine are placed under the skin, be careful to place the lead at the appropriate depth to avoid the risk
of skin erosion.
Erosion of occipital nerve stimulation electrode lead
Minimizing the Possibility of Erosion—Electrode Insertion Plane
Minimizing the Risk of Infection Meticulous aseptic technique, closed gloving Perioperative antibiotics Avoid excessive tissue dissection Meticulous hemostasis Appropriate size of incision
not too small not too large
Avoid over-‐tightening of sutures
Wound edge antisepsis Glove change/clean before handling implant Local gentamicin, triclosan impregnated sutures
PRECAUTION: Infection—Follow proper infection control procedures. Infections related to system implantation might require that the device be explanted.
CE marking does not necessarily indicate regulatory approval status for all markets. Please refer to the instructions for use for a full listing of indications, contraindications, warnings and precautions. Genesis is a trademark of Advanced Neuromodulation Systems, Inc d/b/a St. Jude Medical Neuromodulation Division. ST. JUDE MEDICAL, the nine-squares symbol, and MORE CONTROL. LESS RISK. are trademarks and service marks of St. Jude Medical, Inc. and its related companies.
Safety and Trademark Information
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Right diagnosis Patient education Multimodal treatment Psychological evaluation if necessary Preventive medication (as mentioned above) BOTOX Neuromodulation
143
Management of patients after implantation Zaza Katsarava
Before implantation
The diagnosis was right All conservative options were not successful Illness behavior / secondary benefit was excluded ONS pro/contra were discussed
Realistic goals Possible side effects
After implantation
Am I cured? No you are not Medical treatment should be continued
Our experience
Cen Eur Neurosurg 2011; 72(2): 84-89
ONS Cluster HA in Essen
10 patients with chronic intractable CH Prospective re-evaluation of treatment non response
Chronic Verapamil 450, topiramate 150, Lithium plasma therapeutic range Alone or in combination
Psychological evaluation
ONS Cluster HA in Essen
ONS Cluster HA in Essen
Daily attack frequency 6 (2-14) vs. 3 (0.4-11)
Intensity 8 (6-9) vs. 6 (2-9)
Positive effects
Frequency of cluster attacks declined first 7 patients reduced the number acute medication 7 patients became responsive to oxygen 3 patients decreased preventive medication
Exacerbations
7 patients had a temporary exacerbation bouts lasted between 3-6 weeks Increase of preventive medication Prednisone pulse therapy
Complications
7 patients had a temporary exacerbation bouts lasted between 3-6 weeks Increase of preventive medication Prednisone pulse therapy
neurologist
complications
local infection in one patient Explantation and re-implantation
Dislocation of the electrode in 1 patients
Sensations in a “wrong” place Innervation of muscles
Scare formation around the thoracic connector 1patient
Discomfort Re-operation
complications
Patients with abdominal generator experienced feeling of pressure when they carried heavy objects Patients with gluteal generator experienced feeling of a “foreign body” on an uncomfortable chair
Neurosurgeon
Conclusion
ONS Treatment is a team work
Neurologist Neurosurgeon psychologist Nurse
Pathways for Therapy Success
Dr Denys FONTAINE Hopital Pasteur, Centre Hospitalier Universitaire de Nice FRANCE
Objectives
• to increase the success rate
• to decrease the complication rate
• to manage the eventual complications
• to improve the patient access to therapy
Selection of the patients
• done by a neurologist specialized in headache disorders
• be sure of your diagnosis
• avoid medication overuse headache
• avoid patients looking for secondary benefit
• avoid psychiatric co-morbidities
Information to the patients
• explain the principles / advantages / disadvantages
• device implanted, surgery
• chronic perception of paresthesias
• potential recharge process
• reasonable / realistic expectations
• global rate of improvement : 30 %
• delayed response (several weeks or months)
• attack frequency, days without migraine
• random efficacy
• possibility of complications
• possibility of hardware explantation
• informed consent
Surgery
ELECTRODES IMPLANTATION TECHNIQUES
Principles ONS electrode should overlay the course of the occipital nerve(s) right spot Epifascial plane Anchoring Tunnelization Unilateral / bilateral IPG adapted to your electrode(s) Trained neurosurgeon
Too superficial : skin erosion, lead externalization
Too deep : muscle contraction, spasms, neck stiffness, discomfort
• Attach to the hard underlying fascia Use anchor or sutures placed directly on the
lead without an anchor (but do not use monofilament or polypropylene) • use 2 loops: one in the retromastoid incision and one in the lower cervical incision to allow lead extension during neck movements
• attach the lead above the superior one, and below the inferior one
• avoid sharp bends to avoid lead fracture
Perioperative antibiotics Avoid excessive tissue dissection Meticulous hemostasis Avoid over-‐tightening of the sutures Plan exit site of trial electrodes to avoid crossing the path of permanent device and respect sufficient delay between trial and definitive implantation
respect the patients’ choice (esthetical considerations, preexisting devices, scars, …) and your personal preference one or two step according to the patient operating position anticipate the movements of the neck and trunk / elongation of the lead anticipate the need of recharge process
After the operation
Post-surgical management
• identify early the eventual complications
• do not hesitate to re-operate early in case of migration, infection, hardware dysfunction
• follow up by the neurologist and the surgeon, in close contact
• adaptation of the medication according to the ONS outcome
Patient education
• initial parameters setting by the team : surgeon / neurologist, eventually a clinical nurse and/or company assistant
• use of the remote control use and eventually recharge process
• identify one privileged contact (Nurse +++): telephone number or email address in case of problem with the therapy itself
• especially if patients are referred from far away
Patient journey
• neurologist: identification of candidate patient with CIM • discussion about the therapy, principles, potential benefits and constraints • visit with the surgeon : repetition of the information, surgical risks, consent • surgery • parameters setting : contact and education with the clinical nurse / company
• post op surgeon visit: assessment of eventual complications, compliance with the device / therapy • post op neurologist visit: adaptation of the medication, follow-up
• registry
The surgeon personal point of view
• importance of a multidisciplinary cohesive team (we cannot manage these patients alone)
• recruitment, selection, medication, follow-up neurologist • surgery, surgical complications surgeon • parameters setting, first line safety support clinical nurse
• having a key contact with company who can support and ensure logistics go well
• identify the hardware (labeling is not so clear) and do not change it frequently once you have done your own choice
• this surgery is simple and successful if you follow few rules and avoid the pitfalls
• patients with chronic primary headache are usually less complex to manage than patients with chronic neuropathic pain, but not always
178
Developing referral networks Zaza Katsarava
Headaches
Headache = 80% Migraine = 15-18% TTH = 30-70% Chronic headache 3-4%
WHO’s Global Burden of Disease Study (GBD) 2000
inclusion of migraine, but not tension-type headache
181
Mail/phone interviews
Population-based sample N = 18,000
9968 respondents Response rate = 63.4%
Annual follow-ups
Preventive treatment in Migraine
7% of MIG patients had preventive medication 18% of CM patients had preventive medication
Estimates for 1.000.000 population
About 300-500.000 have occasional headaches 100.000 have migraine 3.000 have chronic daily headache Headaches belong to primary care = GP About 10% should be referred to Neurologist About 10% should be referred to headache specialist
Advocacy for headache patients
GP Neurologists Headache specialists Patients Pharmaceutical companies Governments
Who is interested in what
Patients = suffering / QoL Doctors = patients, ethical, financial ? Companies = ethical / financial Government = ?
Unless increase of productivity is demonstrated
Headache clinics in Georgia
Population 4,435,200 53% urban 47% rural 1,080,000 inhabitants in the Capital City, Tbilisi.
Three headache clinics
Each serving a population of 10.000 people
Medical service and drug supply for 6 months for free
Duration 18 months
OUTCOMES: QoL, Satisfaction and SUSTAINABILITY
Estonia
Population 1,340,000 Intervention place city Tartu
Network of a headache clinic at the Univ. of Tartu and 7 general practitioners
Headache service completely covered by insurance
Education of GPs
Duration 12 months
OUTCOMES: QoL, Satisfaction and SUSTAINABILITY
Bulgaria
Population 7.351.234 Intervention place: 8 regions of the country
Network of a headache clinics at central hospitals general practitioners
Headache service completely covered by insurance
Education of GPs
Duration 24 months
OUTCOMES: QoL, Satisfaction and SUSTAINABILITY
Turkey
Intervention place: A large company with 5000 employees
Screen employees for headache
Offer a headache service in the company office
Complicated cases send to the university of Izmit
Duration 24 months
OUTCOMES: Decrease of lost time and increasing in productivity
Conclusions
Advocacy is need to raise awareness of Patients GP
Referral network is needed Bottom down approach Country / Region dependent
Suggestion
Identify tertiary headache clinic Usually university Headache management is more than implantation
Identify referring region GP Neurologists Patients
Identify people
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