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Pain, Anxiety & Depression:

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1 Pain, Anxiety & Depression:
the aches of the psyche Dr. Ahmed El Missiry DPP Msc (neuro-psych) MD MRCPsych MISAM, LLB Law A Professor of Psychiatry – ASUIP – WHO Consultant Psychiatrist – Kent & Medway NHS Researcher, Neuropsychopharmacology Department Zurich Institute of Technology, Switzerland Regional Representative – Royal College of Psychiatrists (Addiction – KSS)

2 Disclosure In the past three years I received
Honorariums from ApexPharma, Astra Zeneca, BMS, Delta, Janssen Cilag, Lily, Lundbeck, Pfizer, Wyeth Research grants from ApexPharma Advisory ApexPharma, Janssen Cilag, Pharmed International

3 The aches of the psyche …
I do not like my state of mind I'm bitter, querulous, unkind. I am always anxious and tense my thoughts make no sense I dread the dawn's recurrent light; I hate to go to bed at night. I find no peace in paint or type My world is but a lot of tripe. I'm disillusioned, empty-breasted For what I think, I'd be arrested. I am not sick, I am not well My quondam dreams are shot to hell. My soul is crushed, my spirit sore; I do not like me any more. I want to stop this pain … before I turn insane Adapted poems

4 Not knowing where he was, his wife inserted her hands under his clothing and said:
“My brother, no fever in your chest and limbs, but sadness of the heart…” Ebbs Papyrus

5 Greek Mythology THE ALGEA were the spirits of pain and suffering of both body and mind and are related to Oizys, the goddess of misery and sadness, and Penthos the god of mourning and lamentation. Mens Sana en Corpora Sana Decimus Iuvenalis

6 Why Pain, psychological distress (Anxiety and Depression)?
Anxiety, Depression and Pain Symptoms are highly prevalent conditions Lifetime prevalence of Pain = 24-37%1 Lifetime prevalence of Depression = 5-10%2 Lifetime prevalence of Anxiety= 20%2 Anxiety, Depression and Pain complicate each other, affect outcomes, cause more morbidity and disability and increase costs. Regier DA, Myers JK, Kramer M, et al. The NIMH Epidemiologic Catchment Area program: historical context, major objectives, and study population characteristics. Arch Gen Psychiatry.1984;41: Kessler, R.C., S. Zhao, D.G. Blazer, and M. Swartz, Prevalence, correlates, and course of minor depression and major depression in the National Comorbidity Survey. J Affect Disord, (1-2): p

7 “Comorbidity is the rule, not the exception”
Lifetime comorbidity of mood and anxiety disorders “Comorbidity is the rule, not the exception” 1 Kessler et al, Arch Gen Psychiatry 1995; 2 DSM-IV-TR™ 2000; 3 Brawman-Mintzer et al, Am J Psychiatry 1993; 4 Rasmussen et al, J Clin Psychiatry 1992 ; 5Dunner, Depression and Anxiety 2001 DEPRESSION 48% of patients with PTSD1 Up to 65% of patients with Panic Disorder2 67% of patients with Obsessive-Compulsive Disorder4 42% of patients with Generalised Anxiety Disorder3 Up to 70% of patients with Social Anxiety Disorder5 Panic Disorder GAD Social Anxiety Disorder Post-Traumatic Stress Disorder OCD Pain comorbidity= Av 65% Pain

8 topics today Strength of association (D/R – Predictive)
Can Pain be distressing? What is the prevalence of Anxiety & depression in painful disorders? Do depression & anxiety hurt? What is the prevalence of pain symptoms in Anxiety & depression? Does the presence of pain affect recognition and treatment of anxiety / depression? What is the common neurobiological basis of pain/anxiety/ depression? What are the treatments available?

9 Can pain be distressing ?!!
The prevalence of depression in pain disorders [1] In general population pain = 18% (4.7%-22%) In Primary Care clinics = 27% (5.9%-46%) In pain clinics = 52% (1.5%-100%) In orthopedic clinics = 56% (21%-89%) In dental/facial pain clinics = 85% (35%-100%) In gynecology pelvic pain clinics = 13% (12%-17%) Prevalence of anxiety disorders in patients with chronic pain In general population= 35 % [2] back pain clinic = 20% - 57% [3,4] 1- Matthew et al Arch Intern Med. ;163: , 2003 2- Manchikanti et al Pain Physician, Volume 5, Number 2, pp , 2002 3- Sommer 18th European Congress of Psychiatry. February 27, March 2, 2010 4- Moya et al Aten Primaria Sep 15;26(4):

10 The likelihood of anxiety and depression increase with the number of painful symptoms
One thousand adult patients Any Symptom Depression Anxiety N Pain 16 (7) 5 (2) 2 (1) 215 0-1 50 (22) 27 (12) 17 (7) 225 2-3 67 (35) 44 (23) 25 (13) 191 4-5 140 (61) 100 (44) 68 (30) 230 6-8 113 (81) 84 (80) 68 (48) 130 9+ Kroenke K, Spitzer RL, Williams JB, et al. Physical symptoms in primary care: predictors of psychiatric disorders and functional impairment. Arch Fam Med.1994;3:

11 Increasing pain predicts increased Anxiety & Depression
<0.001 N=448 Requited from Primary care <0.001 Blozik et al BMC Musculoskelet Disord Jan 26;10:13.


13 Does Depression Hurt?! The prevalence of pain in depressed ranged from 15% to 100% (mean prevalence, 65%). Patients With Pain, % Study Setting No. of Patients Source 69 Primary care 573 Bair et al 51 Psychiatric inpatients 29 Delaplaine et al 85 Neurology clinic 432 Diamond 59 Outpatient clinic Hollifield et al Private practice 196 Lindsay and Wyckoff 77 Headache 37 chest pain Research institution Mathew et al 56 Psychiatric patients Merskey and Spear 41 22 Pelz et al 65 Depressed outpatients 150 Singhl 43 General practice 28 Vaeroy and Merskey 60 40 von Knorring 57 161 von Knorring et al 100 Respondents to newspaper advertisement 16 Ward et al 15 Watts

14 Chronic Pain in Depression
Does Depression Hurt?! Chronic Pain in Depression subjects representative of the general populations of the United Kingdom, Germany, Italy, Portugal, and Spain. Pain was 4 times more likely in subjects with major depressive disorder (OR 4.0; 95% CI, ) Ohayon & Schatzberg Arch Gen Psychiatry. 2003;60:39-47

15 Does Depression Hurt?! Results from the FINDER study
FINDER was a 6-month prospective, observational study of 3468 outpatients with depression initiating antidepressant treatment. 56.3% experienced mod/severe pain 53.6% had mod/severe pain-related interference with functioning. Demyttenaere et al (2010) Journal of Affective Disorders –60

16 43% of depressed patients experienced chronic painful symptoms1
More Depressive Symptoms … more pain 43% of depressed patients experienced chronic painful symptoms1 Normal mood (n=18,232) 50 Participants with at least 1 depressive symptom (n=3140) †† 40 Depression – 5 DSM-IV criteria met (n=748) 30 Patients (%) †† 20 †† †† * 10 * †† * * Backache GI disease Joint/ articular Headache Limb ache  1 Chronic painful symptom Graph adapted from Ohayon MM, Schatzberg AF. Arch Gen Psychiatry 2003;60: 39–47.

17 Are Pain symptoms a marker for depression?
1,042 consecutive outpatients screened for depression Gerber et al J Gen Intern Med Mar-Apr;7(2):170-3

18 Does Anxiety Hurt?! *** ***
Brandenburg et al. Poster presented at The 25th Annual Conference of the Anxiety Disorders Association of America (ADAA) , March 2005, Seattle, WA, USA

19 Are Pain symptoms a marker for Anxiety?
40 30 20 10 33% 31% 28% 26% anxiety disorders (%) Prevalence in Chest pain Abdominal Headache Fatigue pain Kroenke K et al. Arch Fam Med 1994;3:774–779

20 Does Pain affect the recognition of Anxiety & Depressive disorders?
More than 50% of depressed or anxious patients presenting with pain are not recognized Rates of Recognition of Depression and Anxiety by Style of Clinical Presentation Recognised by Clinician (%) Persistent presented with only somatic & did not believe any psychological cause presented with only somatic symptoms Initial presented with only 1 somatic Initial presented with 1 psychological symptom Kirmayer LJ et al. Am J Psychiatry 1993; 150:

21 Why we can not see the depression and anxiety in pain?
The Central effect Stahl, 2008

22 Why we can not see the pain in depression?
The Central effect Stahl, 2008

23 Difficulty concentrating
Why we can not see the pain? Diagnostic Criterion Bias Symptom Overlap Anxiety* Depression Anxiety Worry Dry mouth Palpitations Sweating Trembling Blushing Stuttering Depressed mood Loss of interest or pleasure Appetite disturbance Worthlessness Suicidal ideation Low self-esteem Agitation Irritability Fatigue Difficulty concentrating Sleep disturbance Muscle tension GI complaints Pain *Symptoms of GAD and SAD. DSM-IV-TR. Washington, DC: American Psychiatric Association; 2000.

24 The Spectrum of Symptoms
Why we can not see the depression? 2- Diagnostic Criterion Bias The Spectrum of Symptoms Physical Symptoms Emotional Symptom Body Aches and Pains Sadness & Tearfulness Headaches Loss of Interest Tiredness and Fatigue Anxiety / Irritability Sexual dysfunction Hopelessness GI Changes Concentration Difficulties Vasomotor changes Negative cognitions & Guilt Suicidal Ideations Sleep Disturbances Appetite \wt changes Psychomotor problems Adapted from DSM-IV APA 1994

25 Affective Spectrum Disorders associated with pain
2- Diagnostic Criterion Bias Affective Spectrum Disorders associated with pain Mood disorders Major depressive disorder Dysthymic disorder Premenstrual dysphoric disorder Bipolar disorder (especially bipolar depression or mixed) Anxiety / neurotic disorders Generalized anxiety disorder Panic disorder Posttraumatic stress disorder Somatization / somatoform pain disorders Painful Functional somatic disorders Fibromyalgia Irritable bowel syndrome Migraine

26 Stahl, 2008

27 Somatization Vs Psycholization:
Why we can not see the depression? 3- Presentation Bias Somatization Vs Psycholization: Cheung (1987) described 3 explanatory models for illness; psychological, somatic, or mixed In depression: 45-95% Report Somatic symptoms only 50% Report unexplained symptoms 11% Denies depression

28 Depression and anxiety are Often Missed when The Presentation is Physical
Adapted from Kirmayer et al AJP1993

29 The effect of poor recognition on the patient’s treatment
Mistreatment Under treatment Decreased treatment efficacy Polypharmacy Increase risk of side effects /drug interactions Increase risk of substance misuse

30 The effect of poor recognition on the treatment outcomes
Increase depression Increase Pain Increase functional disability Decrease quality of Life Increased Relapse Rates Decreased Remission Rates Increase health care utilization Increase suicide rates

31 Pain is an independent risk factor for suicide [8]
Chronic pain associated with increased risk of suicide [1, 2, 3]  Rates of suicidal ideation & attempts [4, 5] Over 30% of chronic pain patients reported suicidal ideation [6] 37% of patients receiving opioid therapy reported suicidal thoughts & 20% an attempt [7]. Mental pain in is associated with   risk of suicide [9]. [1] Fishbain et al Clin J Pain. 1991;7:29–36 [2] Penttinen et al Am J Public Health. 1995;85:1452–1453. [3] Tang et al Psychol Med. 2006;36:575–586 [4] Breslau et al Neurology. 1992;42:392–395. [5] Hinkley et al 1994;9:175–185. [6] Edwards et al Pain. 2006;126:272–279. [7] Saffier et al. K Journal of Substance Abuse Treatment. 2007;33:303–311 [8] Ilgen et al Gen Hosp Psychiatry. 2008; 30(6): 521–527. [9] Van Heeringen et al Psychiatry Res Feb 28;181(2):141-4.

32 “For several years I have been aware of my own mortality, for some strange reason it had been on my mind…Since I have had this deteriorating back problem which causes constant pain and …… a barrier of intimacy … . I had two spinal interventions to cure the pain, I had great disappointment when the first failed, and was devastated when the second failed, ….I was told nothing… I have had one hope and now it is gone …. this feels like the sword of Damocles …. How long it will be another day, month, several months? Before I…..” Jan 2008

33 The biology of Pain Sensory channels: Pain Modulation
Sensory discriminative component Motivational affective component Pain Modulation Spinal Modulation (Gate Theory) Melzack and Wall 1965 Descending inhibitions Opioid system 5HT system NE system Others Descending facilitation

34 Ascending pathways Motivational Affective pathway
Sensory- Discriminatory pathway Stahl, 2008

35 Descending Inhibitory System
Opiate (endorphins) Serotonin Norepenephrine Sympathetic Descending Inhibitory System + + Sub P (NK1,2,3) VIP (VIPR) Somatostatin Calcitonin GABA Glutamate Glycine NMDA NO CCK Stahl, 2008

36 Descending Tracts

37 Possible Explanation: Descending Pathways
PAIN: Depletion of monoamines Increase CRF IL2 – TNF –IL6 DEPRESSION & ANXIETY:  Endogenous Opiates  NE -  5HT  CCK  Sub-P

38 Distress and pain disorders share the same anatomical sites
executive functions & perceived control over pain Process information from sensory to emotional (mood & pain) Rational cognitive functions & pain processing Associative and episodic memories memory of emotional reactions Reward increases in negative affects

39 Induction of Negative Mood Disrupts Emotion Regulation Neurocircuitry and Enhances Pain Unpleasantness Negative or neutral moods were induced in healthy volunteers who underwent heat pain whilst in an fMRI scanner. Pain was rated more unpleasant after the sad mood induction. Depressed mood was associated with increases in negative pain-related cognitions (catastrophizing) Background: Depressed mood alters the pain experience. Yet, despite its clear clinical relevance, little is known about the cognitive and neural mechanisms underlying this phenomenon. We tested an experimental manipulation to unravel the interaction between depressed mood and pain. We hypothesized that dysregulation of the neural circuitry underlying emotion regulation is the mechanism whereby pain processing is affected during depressed mood. Methods: Using functional magnetic resonance imaging, we compared the effects of sad and neutral cognitive mood inductions on affective pain ratings, pain-specific cognitions, and central pain processing of a tonic noxious heat stimulus in 20 healthy volunteers. Results: The increase in negative pain-specific cognitions during depressed mood predicted the perceived increase in pain unpleasantness. Following depressed mood induction, brain responses to noxious thermal stimuli were characterized by increased activity in a broad network including prefrontal areas, subgenual anterior cingulate cortex, and hippocampus, as well as significantly less deactivation when compared with pain responses in a neutral mood. The participants who reported the largest increase in pain unpleasantness after the sad mood induction showed greater inferior frontal gyrus and amygdala activation, linking changes in emotion regulation mechanisms with enhancement of pain affect. Conclusions: Our results informhowdepressedmoodand chronic pain co-occur clinically and may serve to develop and translate effective interventions using pharmacological or psychological treatment. Areas that showed increased activity during pain in the depressed mood state - left insula, thalamus, hippocampus, IFG, dlPFC, OFC, and the sACC. The thalamus and the insular cortex are part of the afferent nociceptive network. dlPFC, dorsolateral prefrontal cortex; IFG, inferior frontal gyrus; OFC, orbitofrontal cortex sACC – subgenual anteria cingulate cortex Berna C et al. Biol Psychiatry 2010;67:

40 Proposed cognitive models
increased negative mood → increased catastrophizing → increased pain unpleasantness Pain related cognitions Increased catastrophizing (rumination) More activity in IFG and amygdalae induced Negative mood explains 34% variability Strong effect Mechanisitic hypothesis: Dysfunction of emotion regulation Increased cognitive load Pain Increased Pain Unpleasantness explains 58% variability No effect Increased activity in the left IFG, dlPFC and OFC Change in neural processing in prefrontal areas Less activity in IFG and amygdalae Berna C et al. Biol Psychiatry 2010;67: dlPFC, dorsolateral prefrontal cortex; IFG, inferior frontal gyrus; OFC, orbitofrontal cortex

41 Depressed patients seen in primary care
How we can help ? Increase Awareness Better identification Proper & early treatment for Neuropathic Pain Proper & early treatment for Depression/anxiety Depressed patients seen in primary care

42 Treatment for Neuropathic Pain
Treatment / control of cause Alternative treatments (TENS, Acupuncture) Pharmacotherapy: NSAID / Pain Killers SNRIs / TCA Anti-epileptics Alpha 2 Delta agonists Opiate Based preparation !! TMS Epidural blocks Implantable drug pumps Neurostimulation surgical interventions Psychological: CBT for Pain

43 Risk of iatrogenic addiction in patients treated with opioids
A systematic review 41 studies with conflicting findings Risk can be relatively high (>10%) or low (<0.1%). [1] A systematic review noted the prevalence of [2] Lifetime SUD 36% to 56% Current SUD 43% Aberrant medication-taking behaviours 5% to 24% Risk factors for opioid abuse in patients with chronic pain are [3]: young age, male gender, past alcohol or cocaine abuse, previous drug conviction, mental health disorders, pain in multiple regions, pain after MVA [1] Wasan et al [2] Martell et al 2007 [3] Højsted & Sjøgren

44 Opioid treatment; may need a revisit
A large population-based study found that opioid usage was significantly associated with: more severe pain, poorer self-rated health, lower quality of life, less physical activity, lower employment, higher levels of health care utilization, and more subjects living alone impaired neuropsychological performance  reaction times, psychomotor speed, and working memory Højsted & Sjøgren Curr Opin Anaesthesiol Oct;20(5):451-5.

45 20-30% partial response (Residual symptom).
Treatment of anxiety and depression (4) Psychosocial and occupational functioning restored Aim at Recovery (3) Sustained absence of symptoms (2) Remission of symptoms Quality of Recovery Symptomatic recovery Syndromal recovery Functional recovery. (1) Response To treatment 20-30% partial response (Residual symptom). Road To Recovery

46 Residual Symptoms Predicts Higher Relapse Rates
20 40 60 80 100 120 1 2 4 6 8 10 12 Months of Follow-up Probability of Remaining Well (% ) Remission (n=41) Residual Symptoms (n=19) Rush AJ, et al Psychiatry Ann. 1995; 25: 704

47 What is the impact of pain on treatment?
The challenge in treatment What is the impact of pain on treatment? Painful Somatic symptoms may be less responsive to treatment relative to other symptoms Depressive symptoms Positive well being Non painful Somatic symptoms Painful Somatic symptoms Greco T et al. J Gen Intern Med 2004; 19:

48 Painful symptoms are associated with worse depression outcome
What is the impact of pain on treatment? the ARTIST Trial Depression outcome at 6 month for n=573 Treated in primary care Painful symptoms are associated with worse depression outcome 458 (80%) have pain 190 (33%) mild pain 165 (29%) moderate pain 103 (18%) severe pain Depressive symptoms Around 60% adequate treatment was given DeVeaugh-Geiss ey al Pain Medicine 2010; 11: 732–741

49 How to achieve recovery?
Proper identification & early treatment for Depression Pharmacotherapy: SNRIs / TCA Mood stabilizers (CBZ) Alpha 2 Delta agonists (pregabalin / Gabalin) BZD Pipe Lines: NMDA Antagonists Somatic Treatment: TMS Psychosocial: CBT for Depression, social inclusion & re-habitation

50 What Antidepressant to Use?
Pooled data from Thase et al & Nemerrof et al

51 What Antidepressant to Use in painful depression?

52 What SNRI to use in Painful Anxiety & Depression?
Duloxetine & Venlafaxine are both effective…. -16 -14 -12 -10 -8 -6 -4 -2 1 2 3 4 6 8 10 12 Least Squares Mean Change Duloxetine (n=318) Venlafaxine XL (n=330) Weeks Duloxetine 60mg OD Duloxetine 60 - 120mg Ven 75mg OD Ven 150mg OD Ven 150 225mg Improvement No significant difference at 6 or 12 weeks Perahia D et al. Comparing Duloxetine and Venlafaxine in the Treatment of Major Depressive Disorder Using a Global Benefit-Risk Approach. New Clinical Drug Evaluation Unit (NCDEU) Florida 2005

53 What Antiepileptic to use?
NNT Anticonvulsant mechanisms of action Reduction of excitatory amino acid activity Modulation of Ca++ Channels Increase in CNS GABA activity Decrease in sodium channel activity Drug 3.3 (2–9.4) + Carbamazepine 3.7 (2.4–8.3) + (?) Gabapentin Lamotrigine 3.0 (2.3–4.5) Topiramate 3.3 (2.3–5.9) Pregabalin Vinik J Clin Endocrinol Metab Aug;90(8):

54 Pregabalin Sibilia Quilici et al BMC Neurology 2009

55 Pregabalin HAM-A score 20 HAM-D score <15 *** *** *** *** *** * **
*** *** *** *** * ** * // D4 EP *P<0.05, **P<0.01, ***P0.001 vs. placebo †P<0.05 vs. venlafaxine Telephone assessment on Day 4. Mean baseline HAM-A ~27.5. Change over time based on MMRM analysis. Endpoint: 8 weeks (LOCF, ANCOVA) Herman et al. CINP 2008

56 Ά2δ(pregabalin) TCA - Miratzepine Treatment
SSRI ?? SNRI Ά2δ(pregabalin) TCA Miratzepine CBZ – Lamotrogine – Tiagabine

57 What other interventions to use?
Psychological Uses Behavioural Increase exercise/activity levels; overcome fear–avoidance Cognitive-behavioural Reduce depression and anxiety associated with pain; develop effective coping strategies; reduce problematic cognitive styles. Interpersonal Address role transitions due to pain; relationship difficulties/conflicts Adjunctive techniques Biofeedback Muscle relaxation; control of physiological parameters contributing to pain (e.g., headache) Guided imagery Relaxation; distraction from pain Hypnosis Relaxation; pain severity reduction; distraction Progressive muscle relaxation Muscle relaxation; distraction from pain

58 Conclusion: Despite the frequent coexistence of depression , anxiety and pain the magnitude and implications of that relationship are still unclear. Neglecting the treatment of fatigue, low energy , and painful physical symptoms in depressed patients can lead to unsatisfactory outcomes, characterized by a failure of depressed patients to return to normal social and occupational functioning. Keller MB et al 1992 , Judd LL et all 1998, Angst J 1992and Kupfer DJ 1991; Sheline YI et al 1996; Blier P et al. 2001


60 THANKS Dr. Ahmed El Missiry A Professor of Psychiatry – ASUIP – WHO
DPP Msc (neuro-psych) MD MRCPsych MISAM, LLB Law A Professor of Psychiatry – ASUIP – WHO Consultant Psychiatrist – Kent & Medway NHS Researcher, Neuropsychopharmacology Department Zurich Institute of Technology, Switzerland Royal College of Psychiatrists Regional Representative KSS – Addiction Office: Pagoda CMHC Hermitage Lane, Barming Maidstone. Kent ME16 9PD Tel: Mobile:

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