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  1. 1.   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
  2. 2. ICHD-­‐II  Diagnostic  Criteria   Episodic  attacks  of  headache  lasting  4-­‐72  hours  with  the  following   features:   Headache has at least two of the following During headache at least one of the following: characteristics: Nausea and/or vomiting Unilateral location Photophobia and phonophobia Pulsating quality Moderate or severe pain intensity Aggravation by routine physical activity Further  sub-­‐classified  on  basis  of  frequency  of  headaches   Episodic  migraine  <15  days/month   Chronic  migraine    >15  days/month    
  3. 3. Phases  of  Migraine   Time   Premonitory  Aura   Headache  &   Resolution   Associated  Features  
  4. 4. Complex  array  of   Aura  symptoms  occur  with   symptoms  reflecting  focal   headache:   cortical  or  brainstem   – Always     18%   dysfunction   – Sometimes   13%   – Never       Gradual  evolution     69%     5-­‐30minutes  (<60minutes)   Types  of  aura:     – Visual     99%   Usually  before  headache;     – Sensory     31%     can  be  during  or  even   – Language   18%   after  headache   – Motor      6%    
  5. 5. Pain:   • Unilateral  or  bilateral   • Throbbing,  worsened  by  movement  or   activity   • Cutaneous  allodynia   • Neck  stiffness/pain  (80%)     Associated   Sensory  hyperexcitability   Symptoms:   • Photophobia,  phonophobia,  osmophobia     • Motion  sensitivity/vertigo     Gastrointestinal  disturbance   • Nausea/Vomiting/Diarrhoea     MIGRAINE  IS  A  FEATUREFUL  HEADACHE  
  6. 6. ICHD-­‐IIR  DIAGNOSTIC  CRITERIA   Migraine headache occurring on of medication overuse, not attributed to another disorder. On During headache at least one has at least two of the following characteristics: of the following: Unilateral location Nausea and/or vomiting Pulsating quality Photophobia and phonophobia Moderate or severe pain intensity and/or treated and relieved by triptan(s) or ergot before developing into a migraine Aggravation by routine physical activity 1. ICHD 2006 Headache Classification Committee of the International Headache Society. Olesen J et al. Cephalalgia 2006;26:742
  7. 7. 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   European Union Migraine 50M Chronic Medically Refractory Migraine Chronic Migraine 7.3M 1M? 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.  
  8. 8.     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   1.  Menken M,Munsat T, Toole J. Archives of Neurology 2000; 57:418-420.   2.  Lipton  RB  et  al.  Headache.  2001.    
  9. 9. 91%  of  migraine  patients  report  disability   Work/School  Productivity   51%   Reduced  by   50%   Unable  to  Do  Chores/   76%   Household  Work   Household  Work  Productivity   67%   Reduced  by   50%   Missed  Family/Social   59%   Leisure  Activity   0%   20%   40%   60%   80%   100%   Lipton  RB  et  al.  Headache.  2001.  
  10. 10.     Affects  1.4-­‐2.2%  of  people  wordwide1   Significantly  more  burdensome  than  episodic   migraine:2   80     70   71.7   * 67.2   61.4   * 60   56.5   * Mean  MSQ  score   48.3   50   44.4   40   Chronic  migraine   30   Episodic  migraine   20   *  P<0.0001   10   0   Unable  to  perform  normal   Difficult  to  perform   Emotional  effects   activities   normal  activities   1. Natoli  JL,  et  al.  Cephalagia  2010;30:599-­‐609.   2. Blumenthal  AM  et  al  Lancet  2010    
  11. 11. Migraine  is  an  important  public  health  problem   that  is  associated  with  substantial  costs1–3   Direct costs Indirect costs Medication Absence from work (absenteeism) Reduced productivity at work Consultation (presenteeism) Hospital admission Lost career opportunities Diagnostic investigations Unemployment 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  
  12. 12.   Aura:  Pathophysiological  Hypotheses       Wolff’s  vascular  hypothesis   Cortical  spreading  depression  of  Leao         Migraine  aura  secondary  to  cerebral   Wave  of  excitation  followed  by  inhibition  that   hypoxia   traverses  the  cortex  at  3-­‐6  mm/min         Hyperperfusion   Normal     CBF   Hypo-­‐   perfusion   Aura   Headache   2   4   6   8   10   12   Hours  after  angiography   Leao. J. Neurophysiol. 1944; Leao and Morison. J. Neurophysiol. 1945 Wolff. Headache and other head pain. 1963   Silberstein SD et al. Headache in Clinical Practice. 2nd ed. 2002
  13. 13.   Xenon-­‐133  Studies       Relative  timing  of  CBF,  Aura  and   Headache   Hyperperfusion   Normal     CBF   Hypo-­‐   perfusion   Aura   Headache   2   4   6   8   10   12   Hours  after  angiography   Olesen et al, Ann Neurol 1990; Olesen, Migraine and other headaches: the vascular mechanisms. 1991; Olesen, The headaches. 1993
  14. 14.   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       Hadjikhani et al, PNAS 2001 Cortical  spreading  depression  rather  than  vasoconstriction  is  the  basis  of  aura  
  15. 15. Specific  dorsal  rostral  pontine  activation  in  migraine   Spontaneous Spontaneous Chronic Episodic Migraine Episodic Migraine Migraine Weiller et al, Nature 1995 Afridi et al, Arch Neurol 2005 Matharu et al, Brain 2004
  16. 16. CSD-­‐triggered  Trigeminovascular  Activation?   Visually-­‐triggered  Migraine     BOLD-­‐fMRI  Study   Meninges Trigeminal nerve Sphenopalatin e ganglion Trigeminal ganglion Pain Cao et al, Arch Neurol 1999; Cao et al, Neurology 2002 Superior salivatory nucleus Trigeminal BOLD  signal  changes  in  brainstem   nucleus before  occipital  cortex  signal  changes   Adapted from (consistent  with  CSD)  or  onset  of  visual   Iadecola C. Nat Med 2002; Bolay H et al. Nat Med. 2002. symptoms  
  17. 17.   Abnormal  cortical   Abnormal  brain  stem   activity   function   Hyperexcitable  brain   Excitation  of  brain   ( Ca++,   Glu,   Mg++)   stem,  PAG,  etc.   Cortical  Spreading  Depression   Activation/Sensitization  of  TGVS   Headache   Pain   Vasodilation   Central  Sensitization   Neurogenic     Inflammation     TGVS=trigemino-­‐vascular  system.   Adapted  from  Pietrobon  D,  Striessnig  J.  Nat  Rev  Neurosci.  2003;4:386-­‐398.  
  18. 18.   Pharmacological   Treatments   Lifestyle   modification   Psychological   and  trigger   and  behavioural   management   treatments   Education  and   Headache   Surgical   Support     Management   treatments  
  19. 19. • 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   90   80   70   Percentage  of  patients   60   50   40   30   20   10   0   Stress   Hormones   Missed   Weather   Sleep     Perfume   Neck   Lights   Alcohol   Smoke   Sleeping   Heat   Food   meals   disturbance   /odours   pain   late   Triggers   1. Kelman L. Cephalalgia 2007;27:394–402.
  20. 20.   Pharmacological   Treatments   Lifestyle   modification   Psychological   and  trigger   and  behavioural   management   treatments   Education  and   Headache   Surgical   Support     Management   treatments  
  21. 21. Non-­‐specific  Treatments   Specific  Treatments   • Paracetamol  1g   • Triptans:   • NSAIDs  (high-­‐dose  &  soluble):   Sumatriptan     Aspirin  600-­‐900mgs   Rizatriptan   Ibuprofen  600-­‐800mgs   Zolmitriptan     Naproxen  500-­‐1000mgs   Almotriptan     Tolfenamic  acid  200mgs   Eletriptan     Diclofenac  50-­‐75mgs   Naratriptan     • Opioids   Frovatriptan   • Use  concurrently  with  Prokinetics:   • Ergot  derivatives:   Domperidone  10-­‐20mgs   Ergotamine  1-­‐2mg  tablet  or   Metoclopramide  10mgs   suppository   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   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  
  22. 22. 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 .
  23. 23. 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  
  24. 24. Medication overuse1,2* Preventative therapy Detoxification FAIL * 15 days/month: simple analgesics, combinations of drugs; or 10 days/month: combination analgesics, ergotamines, triptans, opioids, barbiturates. 1. Diener HC, Limmroth V. Lancet Neurol 2004;3:475–483. 2. Katsarava Z et al. Curr Neurol Neurosci Rep 2009;9:115–119.
  25. 25. Out-­‐patient  Setting   Day  Case  or  In-­‐patient  Setting   • Beta-­‐blockers   • Botox   – Propranolol   • Greater  occipital  nerve  blocks   • Antidepressants   • Intravenous  dihydroergotamine  infusions   – 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  
  26. 26.   Pharmacological   Treatments   Lifestyle   modification   Psychological   and  trigger   and  behavioural   management   treatments   Education  and   Headache   Surgical   Support     Management   treatments  
  27. 27. 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          
  28. 28.  
  29. 29.   DEFINITION       • 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  
  30. 30. CAUSES   After  secondary   causes  are  ruled  out   Primary  headache   disorders   Chronic  daily  headache   Episodic  headache   Frequency     Frequency  <15  days/month   Short-­‐duration  chronic   Long-­‐duration  chronic     daily  headache   daily  headache   With  or  without   Duration  <4  hours  or  multiple   Daily  or  near-­‐daily  headache   medication  overuse   discrete  episodes   lasting     Chronic  tension-­‐   New  daily   Hemicrania   Chronic  migraine   type  headache   persistent  headache   continua   1.  Silberstein  SD  et  al.  Neurology  1996;47:871  
  31. 31. 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.
  32. 32. 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
  33. 33.   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
  34. 34.   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.
  35. 35.   PRIMARY  HEADACHES   SECONDARY  HEADACHES       Chronic  migraine   Occipital  neuralgia   Chronic  cluster  headache   Cervicogenic  headache   Hemicrania  continua   Post-­‐traumatic  headache   SUNCT    
  36. 36.   • Open  Label  series   • ONSTIM  Study   • PRISM  Study   • St  Jude  Medical  Study  
  37. 37. OPEN  LABEL  CASE  SERIES       Author   Number   Mean  duration   Number   Follow  up     of  disorder   improved  (>50%)   (yrs)   (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%)   Medication overuse probably negatively affects outcome Popeney& Alo Headache 2003; Oh et al. Neuromodulation 2004; Schwedt et al Cephalalgia 2007; Matharu et al Brain 2004
  38. 38. Occipital  Nerve  Stimulation  for  the  Treatment  of  Intractable   Chronic  Migraine  Headache     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     Saper JR, et al Cephalalgia. 2011;31(3):271-285.  
  39. 39. This prospective, randomized, double-blind, controlled study examined the efficacy and safety of occipital nerve stimulation in adult chronic migraine patients. Adjustable Stimulation (AS) Patients (Active, N=29 completed) enrolled who responded to an occipital nerve block Preset Stimulation (PS) 2:1:1 ratio (Control, N=16 completed) Medical Management (MM) (Comparator, N=17 completed) 12 Weeks
  40. 40. Mean percent reduction (SD) Mean (SD) reductions in actual in headache days per month headache days per month Baseline   22.4+6.3   23.4+5.1   23.7+4.3   30%   8   27.0%   7   25%   (44.8) 6.7   6   (10.0) 20%   5   15%   4   3   10%   8.8%   2   (28.6)   5%   1   1.5   4.4%   (4.6) 1   (19.1)   (4.2) 0%   0   Adjustable   Preset   Medical   Adjustable   Preset   Medical   Stimulation  (AS)   Stimulation  (PS)   Management   Stimulation  (AS)   Stimulation  (PS)   Management   (MM)   (MM)  
  41. 41. Reduction (SD) in Responder rates overall pain intensity 2   50%   40%   1.5   1.6 39%   30%   1   20%   0.5   0.5 0.6 10%   6%   0%   0   0%   Adjustable   Preset   Medical   Adjustable   Preset   Medical   Stimulation  (AS)  Stimulation  (PS)   Management   Stimulation  (AS)   Stimulation  (PS)   Management   (MM)   (MM)  
  42. 42. Fifty-six device-related adverse events occurred in 36 out of 51 patients. Adverse  Events   %   Adverse  Events   %   Lead migration/dislodgement   24%   Implant site (IPG) hematoma   2%   Therapeutic product ineffective   16%   Implant site (IPG) irritation   2%   Implant site (lead/extension tract) Implant site (lead/extension tract) 14%   2%   infection   inflammation   Incision site complications   8%   Lead fracture   2%   Implant site (IPG) infection   4%   Migraine   2%   Implant site (IPG) pain   4%   Post-procedural nausea   2%   Neck pain   4%   Post-procedural pain   2%   Burning sensation   2%   Rash   2%   Discomfort   2%   Sensation of pressure   2%   Extension migration/dislodgement   2%   Stitch abscess   2%   High impedance   2%   Suture-related complications   2%   Hypotension   2%   Tenderness   2%  
  43. 43.     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.     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    
  44. 44. 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. Patients enrolled Active Stimulation 1:1 ratio Trial stimulation to Two-year follow-up assess its predictive conducted to assess value safety. Sham Stimulation (Control) 5–10 days 12 Weeks
  45. 45. Primary efficacy measure: reduction in migraine days per month Mean reduction (SD) in Mean percent reduction in migraine days per month migraine days per month 6   100%   90%   5.5   5   (8.7) 80%   70%   4   3.9   60%   3   (8.2) 50%   40%   2   30%   20%   27%   1   20%   10%   0   0%   Active  Stimulation   Sham  Stimulation   Active  Stimulation   Sham  Stimulation  
  46. 46. A two-year follow-up was conducted to assess safety. Complications included the following: 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%  
  47. 47. 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  
  48. 48. 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    
  49. 49. Patient Enrolled Group A: Active PNS Implanted 2:1 Ratio Randomize and Device Activation Group B: Control (Blind) 80-­‐  to  90-­‐day  roll  in   4-­‐week  visit   12-­‐week  visit   24-­‐week  visit   52-­‐week  visit   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.
  50. 50.   Primary  Outcome   50%  VAS  reduction  with  no  increase  in  average  headache  frequency  or  duration   18   16   P=0.21   14   12   10   8   6   4   2   0   Active   Sham  
  51. 51. Continuous Proportion Responder Analysis Based on Mean Daily Average Pain Intensity VAS Measurements With No Increase in Average Headache Frequency or Duration met   Control  Group   Active  Group   %  reduction   protocol   %  responders   %  responders   p-­‐value1 Patients  Achieving  Various  Levels  of  Pain  Relief     from  baseline objective     (n=52) (n=105) (>10%  dif.)2 100%   0,0% 38,5% 69,5% <0,001 Yes Percentage  of  Patients   10,0% 30,8% 58,1% 0,001 Yes 80%   20,0% 19,2% 41,9% 0,005 Yes 60%   30,0% 17,3% 37,1% 0,011 Yes 40%   40,0% 15,4% 25,7% 0,143 No 50,0% 13,5% 17,1% 0,553 No 20%   60,0% 9,6% 11,4% 0,731 No 0%   70,0% 1,9% 4,8% 0,664 No 0%   20%   40%   60%   80%   100%   80,0% 1,9% 3,8% 1 No Percentage  of  Pain  Reduction   90,0% 0,0% 1,0% 1 No Control  (n=52)   Active  (n=105)   100,0%         1 Two-sided test of no difference 2 One-sided lower 95% confidence bound Significance demonstrated at 30% reduction in pain (p-value=0.011)
  52. 52. 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. Mean Baseline and Change From Baseline in Headache Days per month—Last Value Carried Forward 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) 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)
  53. 53. 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. Mean Baseline and Change From Baseline in Daily Average Pain Intensity VAS Measurements By Visit —Last Value Carried Forward 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) 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).
  54. 54. The Migraine Disability Assessment (MIDAS) is a questionnaire which measures headache-related disability during the previous 90 days based on five disability questions. Mean Baseline and Change From Baseline in the MIDAS Headache Questionnaire Sum of Items 1 – 5—Last Value Carried Forward 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) 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).
  55. 55. The differences reported between the Active and Control Groups for both measures were statistically significant (p<0,001). Percentage  of  Pain  Relief  Since  Surgery     Percentage  of  Patients  Satisfied   With  Headache  Relief   100%   100%   80%   80%   60%   60%   51,4%   42,1%   40%   40%   17,2%   19,2%   20%   20%   0%   0%   Control  Group  (n=52)   Active  Group  (n=105)   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.
  56. 56. 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. Total   Total   Adverse  Event  +   (N=153)   Adverse  Event  +   (N=153)   n  (%)   n  (%)   Lack  of  efficacy/return  of  symptoms   15  (9,8%)   Nausea/vomiting   3  (2,0%)   Persistent  pain  and/or  numbness  at  IPG/lead  site   15  (9,8%)   Expected  post-­‐op  pain/numbness  at  IPG/lead   2  (1,3%)   site   Normal  battery  depletion   12  (7,8%)   Skin  erosion   2  (1,3%)   Unintended  stimulation  effects   10  (6,5%)   Hematoma   1  (0,7%)   Lead  migration   9  (5,9%)   Seroma   1  (0,7%)   Battery  failure   8  (5,2%)   Wound  site  complications   1  (0,7%)   Lead  breakage/fracture   5  (3,3%)   Pain  or  swelling  at  IPG  site–trauma-­‐related   1  (0,7%)   Infection   4  (2,6%)   Allergic  reaction  to  surgical  materials     1  (0,7%)   Battery  passivation   3  (2,0%)   Device  malfunction–IPG   1  (0,7%)   Device  malfunction–programmer   3  (2,0%)   IPG  migration   1  (0,7%)  
  57. 57. MECHANISM  OF  ACTION       Anatomical Convergence of Trigeminal and Cervical input  
  58. 58. MECHANISM  OF  ACTION       Functional Convergence of Trigeminal and Cervical input   Bartsch et al, Brain 2002
  59. 59. 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
  60. 60. 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
  61. 61. 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.  
  62. 62.  
  63. 63. 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. Total   Category   Adverse  Event  +   (N=153)   n  (%)   Patients  with  one  or  more  anticipated  AE   76   Normal  battery  depletion   12  (7,8%)   Lead  migration   9  (5,9%)   Battery  failure   8  (5,2%)   Hardware-­‐Related   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%)   Lack  of  efficacy/return  of  symptoms   15  (9,8%)   Stimulation-­‐Related   Unintended  stimulation  effects   10  (6,5%)   Nausea/vomiting   3  (2,0%)  
  64. 64. 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. Total   Category   Adverse  Event  +   (N=153)   n  (%)   Patients  with  one  or  more  anticipated  AE   76   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%)   Biological   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%)  
  65. 65. 65 Patient  selection  for   successful  therapy         Zaza  Katsarava  
  66. 66. Headaches Headache = 80% Migraine = 15-18% TTH = 30-70% Chronic headache 3-4%
  67. 67. Chronic Headache Chronic Headache = HA The reasons to define chronic vs. episodic HA Individual burden Burden of social environment Co-morbidities Costs
  68. 68. Chronic Headache The prevalence of chronic headache is about 3-4% For systemic review see Stovner et al, 2006
  69. 69. 69 After Secondary Causes Are Ruled Out Primary Headache Disorders Chronic Headache Episodic Headache Frequency Frequency <15 days/month days/month Chronic  Daily   Short-Duration Headache  (Long   Chronic Daily With or Without Headache Duration)   Medication Duration <4 hours or Daily  or  near-­‐daily   Overuse multiple discrete episodes headache     lasting     Chronic New Daily Chronic Tension- Hemicrania Persistent Migraine Type Continua Headache Headache Silberstein  SD  et  al.  Neurology.  1996;47:871-­‐875.   Dodick  D.  N  Engl  J  Med.  2006;354:158-­‐165.  
  70. 70. 70 CM  =  migraine  on   15  days/month     CTTH  =  TTH  on   15  days/month      
  71. 71. Visual analogue scale 71 Visual analogue scale
  72. 72. Visual analogue scale 72 Visual analogue scale
  73. 73. 73 Migraine With With migraine migraine Visual analogue scale features features Without Without migraine migraine fetures features Triptan TTH? Abortive Migraine? TTH Abortive Migraine time
  74. 74. 74 IHS  2004,   CM  =  migraine  on   15  days/month   No  medication  overuse     Diary  is  needed   Rely  on  patients  recall   Too  restrictive      
  75. 75. 75 IHS  2006,   CM  =     Migraine   HA  on     8  HA  days  is  migraine   No  medication  overuse        
  76. 76. 76 Allergan,  PREEMPT,   CM  =     Migraine   HA  on     50%  is  migraine        
  77. 77. 77 American  way  to  do  it,  Silberstein-­‐Lipton   CM  =     Migraine   HA  on       No  diary  is  needed      
  78. 78. 78 Population-based sample N = 18,000 Mail/phone interviews 9968 respondents Response rate = 63.4% Annual follow-ups
  79. 79. 79 Chronic Migraine definition PREEMPT ( migrainous) Chronic Migraine definition IHS, 2006 ( migrainous) ICHD-2 definition2 0.4% Chronic Migraine definition S-L 0.5% ( migrainous) 1.9% Silberstein-Lipton Criteria3 Chronic Daily Headache 1. Katsarava et al. Cephalalgia, 2011. 2.8% ( 2. Olesen J et al. Cephalalgia. 2006;26(6):742-746. 3. Silberstein SD et al. Headache. 1994;34:1-7.
  80. 80. CM according to S-L = 185 IHS MIG criteria IHS CM = 45 The rest, 185 – 45 = 140 TTH criteria IHS TTH = 40 What is the rest? N = 100
  81. 81. 81 CM  is  NOT  just  more  MIG    
  82. 82. 82 Low   Medication   Definition   Females   Age   BMI   Education   Overuse*   CM-­‐I  (   70%   44   26.4   70%   27%   CM-­‐II  ( 69%   45   26.5   73%   31%   migrainous,  including  overuse)   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 GHC = German Headache Consortium. 2008. Abstract.
  83. 83. 83 70 * 60 Chronic  migraine Episodic  migraine * * 50 41 40 * * * * * % 31 30 30 * 26 * * 19 20 15 10 0 Allergies  or   Sinusitis Asthma Bronchitis Depression Chronic   Anxiety High  Blood   High   Obesity Arthritis Hay  Fever Pain Pressure Cholesterol • Chronic migraine was defined as reported ICHD-2 diagnosis of migraine and days/month *p<0.05. Data from the American Migraine Prevalence and Prevention (AMPP) study. Buse D et al. J Neurol Neurosurg Psychiatry. 2010; In press.
  84. 84. 84 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    
  85. 85. 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. 86. 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. 87. 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  
  88. 88. Central  sensitization   Blink  reflex  and  pain  evoked   potentials  in  MOH     Transient  increase,  normalizing   again  after  withdrawal   (Ayzenberg  et  al.  2006)   50 45 40 35 30 25 20 15 10 Tr A n Tr A n C Ep rols na M na M on ip ip m ta lg OH ta lg OH t ig es es ra ic ic in s M e M O O H H
  89. 89. 1.  Central  disinhibition       2. Stimulation of 6.  PAIN   meningeal sensory nerve (trigeminal) 3. Release of Thalamus   pain- Nerve   enhancing TNC   Vessel     dilation   neuropeptid es, such as Spinothala 5. Activation of Peptide     CGRPTrige mic cortical pain release   minal Inflammation   track centers via TrigeminGangli al  Nerve   on thalamus 4. Activation of trigeminal nucleus caudalis can result in central sensitization 1. Pietrobon D et al. Nat Rev Neurosci. 2003;4:386- CGRP = calcitonin gene-related peptide; TNC = trigeminal nucleus 398. candalis. 2. Pietrobon D. Neuroscientist. 2005;11:373-386.
  90. 90. Post-traumatischer Kopfschmerz Reversible  VBM  changes  in  chronic  posttraumatic   headache  
  91. 91. 91 Low- High- frequency frequency Chronic No migraine episodic episodic migraine migraine migraine 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   1. Lipton RB. Neurology. 2009;72:S3-S7. 2. Bigal ME, Lipton RB. Curr Opin Neurology 2008;21:301-308.
  92. 92. Right diagnosis Multimodal approach Patient education Psychological co-morbidities Physiotherapy Stop medication overuse (if any) Preventive medication Topiramate, BOTOX Betablockers, Valproate etc.
  93. 93. Right diagnosis Do not miss secondary headache Do not mix CM and CTTH Do not miss MOH Do consider psychiatric co-morbidities
  94. 94. Chronic headache with medication overuse ??? Medication overuse headache
  95. 95. 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.    ………….  
  96. 96. Medication Overuse1,2 Preventive Therapy Detoxification * 15 days/month: simple analgesics, combinations of drugs; or 10 days/month: 1. Diener HC, Limmroth V. Lancet Neurol. 2004;3:475-483. combination analgesics, ergotamines, triptans, opioids, barbiturates. 2. Katsarava Z et al. Curr Neurol Neurosci Rep. 2009, 9:115-119.
  97. 97. Education Withdrawal Preventive medication Psychological treatment Follow up
  98. 98. Single analgesic Ergotamines Triptans Combination analgesics 3 Patients With Headache (%) 100 90 Headache Intensity 80 2 70 60 50 40 1 30 20 10 0 0 1 2 3 4 5 6 7 8 9 1011121314 1 2 3 4 5 6 7 8 9 1011121314 Days of Withdrawal Therapy Days of Withdrawal Therapy Diener HC, Limmroth V. Lancet Neurol. 2004;3:475-483.
  99. 99. Controls Abrupt withdrawal Controls Abrupt withdrawal Prophylaxis only Prophylaxis only No. of Headache Days/Month 30 from the start from the start 60 Headache Days/Month Patients Exhibiting a P = 0.01 25 50% Reduction in 50 20 40 (%) 15 30 10 20 5 10 0 0 0 1 2 3 4 5 6 7 8 9 10 11 12 Month 3 Month 5 Month 12 Months Following Withdrawal Months Following Withdrawal Hagen K et al. Cephalalgia. 2009;29:221-232.
  100. 100. 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
  101. 101. 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
  102. 102. Topiramate Efficacy Mean Change in Headache Days Primary 2 Placebo Topiramate endpoint 0.7 1 0.5 0.1 0.2 0 -1 -0.6 -2 -3 -2.9 -3.0* -4 -3.5* -5 -4.7** -6 * p < 0.05 vs placebo -5.4** ** p < 0.01 vs placebo Wk 4 Wk 8 Wk 12 Wk 16 Last 4 wks Patien 26 25 20 15 27 ts 32 30 25 24 32
  103. 103. BOTOX Efficacy Mean Change in Headache Days
  104. 104. 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
  105. 105. 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  
  106. 106. 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  
  107. 107. 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  
  108. 108. 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  
  109. 109. 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  
  110. 110. 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  
  111. 111. 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  
  112. 112. Lead  Placement  (Anchor  Midline)  
  113. 113. 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  
  114. 114.  
  115. 115. 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”  
  116. 116. Technique  first  described  for   Occipital  Neuralgia    
  117. 117. Then  for  Transformed  (Chronic)   Migraine  
  118. 118. Lead  Placement  (Anchor  at   Mastoid)  
  119. 119. Procedural  Details  
  120. 120. Procedural  Details  
  121. 121. Procedural  Details  
  122. 122. 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)  
  123. 123. 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.
  124. 124. 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%)
  125. 125. “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
  126. 126. Extreme  “Out”  Migration   “Extreme” migration of occipital nerve stimulation electrode lead The electrode lead has migrated all the way toward the generator pocket
  127. 127.  
  128. 128.  
  129. 129. “In”  Migration   A. B. “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
  130. 130. Insertion  Plane   Too  Deep   Too  Superficial  
  131. 131. Skin  Erosion   Erosion of occipital nerve stimulation electrode lead 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.
  132. 132.   Minimizing  the  Possibility  of   Erosion—Electrode  Insertion   Plane    

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