fibromyalgia novel therapies, and omt · 2018-10-08 · complex etiology: genetic factors •strong...
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Fibromyalgia RECENT ADVANCES, NOVEL THERAPIES,
AND OMT
Siddharth S. Arora, DO, MS
Pain Medicine Fellow
Larkin Hospital/Nova Southeastern University
February 23rd, 2017
Pain Management as a Psychiatrist
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Conflict of Interest
• None
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Key Points to Cover
1. Complex etiology involving biological and environmental influences
2. Central Sensitization
3. Pathophysiology supported by imaging studies
4. FM vs SSD and the new DSM-V criteria
5. Traditional treatment and novel therapeutic approaches under investigation
6. OMT and Soft Tissue Techniques
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Modern Definition
• Chronic, multifaceted, and widespread musculoskeletal pain syndrome involving both central and peripheral sensitization.
• Assoc w/ spectrum of symptoms
• Affects many domains of functioning: somatic and psychological
• Not same as anxiety and MDD (1)
• Billable Codes: • ICD9: 729.1 “Myositis and Myalgia, unspecified”
• ICD10: M79.7 “Fibromyalgia”
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Early Descriptions
“I, too, have been assigned months of futility, long and weary nights of misery. When I go to bed, I think,`When will it be morning?' But the night drags on, and I toss till dawn...Depression haunts my days. My weary nights are filled with pain as though something were relentlessly gnawing at my bones.”
- Job 7:3-4; 30:16-17 - NLT
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History
1600s 1816 1824 1904 1972 1975 1976 1981 1987 1990 1990s 2007
5
French physician Guillaume
de Baillou: FM-like
symptoms first given a
name: muscular rheumatism
Dr. Balfour described
tender points
Dr. William Balfour,
surgeon at the Univ of
Edinburgh, gave first full
description of FM
Sir William Gowers
coined the term fibrositis
(= inflammation of
fibers) to denote the
tender points found in
patients with muscular
rheumatism
Dr. Hugh Smythe laid the foundation for the
modern definition of FM by describing
widespread pain and tender points
The first sleep EEG study identifying
the sleep disturbances that
accompany FM was performed
No evidence of inflammation so
changed name from fibrositis to
FM (= pain in muscles and tissues)
The first controlled clinical
study with validation of known
symptoms and tender points was
published
The AMA recognized FM as
a real physical condition
The ACR developed
diagnostic criteria for
FM for research. Later
used in clinical practice
FDA approves first
drug for FM: lyrica
(pregabalin)
Concept of neurohormonal
mechanisms with central
sensitization was
developed
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Epidemiology
• Affects 2-8% of US population (2-4)
• Most common cause of widespread MSK pain in women 20-55yo (5)
• Rheum: second to OA as the most common disorder encountered (6)
• Onset: 35-55yo (7)
• Prevalence increases w/age,8 but it can also be seen in children (9-
10)
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Epidemiology
• Children born prematurely – more likely to show tender points and decr pain threshold vs children delivered term (10) (Buskila, et. al.) • case-control study; 60 pre-term and 60 term
adolescents
• observed in both sexes, but girls had > pain sensitivities than boys
• Higher somatic pain sensitivities higher risk of future pain syndromes?
• more studies needed
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Epidemiology
• Buskila, et. al hypotheses: • Differences in pain perception d/t:
• lack of myelination of their sensitive fiber
• immature cortical organization of the somatosensory system
• Differences in pain threshold d/t:
• lack of protection of spinal and supraspinal inhibitory pathways
• abnormal behavioral imprinting 2/2 early painful stimuli increased plasticity of neonatal brain future incr vulnerability of CNS to stress and pain d/o
8
Painful stimuli
perceived as
widespread
and durable
Lower pain
threshold
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Epidemiology: Painful procedures in the NICU 9
• Diagnostic: • Venipuncture
• Heel lancing
• Lumbar puncture
• ROP examination
• Endoscopy
• Bronchoscopy
• Suprapubic bladder tap
• Therapeutic: • Bladder catheterization
• Central line insertion and removal
• Chest tube insertion and removal
• Chest physiotherapy
• Mechanical ventilation
• Dressing change
• Gavage tube insertion
• Intramuscular injection
• Peripheral venous catheterization
• Tracheal intubation and extubation
• Tracheal suctioning
• Suture removal
• Ventricular tap
• Surgical: • Circumcision
• Others
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Epidemiology
• Long term effects of untreated pain in the neonate: • Untreated pain leads to abnormal pain
pathways alteration in cerebral neuroanatomy ?developmental delays, ?emotional disorders, ?chronic pain d/o
• MRI of newborns (within first 7 days of life)
• fMRI’s of newborns: reveal neural activity of pain overlap with adult pain (33)
• Areas: primary somatosensory cortices, ACC, bilateral thalamus, insula
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Complex Etiology
11
Genetic factors
Environmental triggers
Alterations in gene
expression
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Complex Etiology: Genetic factors
• Strong genetic predisposition d/t marked familial aggregation (11-15)
• 1st-degree relatives of pts w/FM: 8-fold increase in risk of FM (16)
• Family members of FM pts: more likely to have lower pain threshold than general pop; often carry dx of other chronic pain syndromes: IBS, TMJ, and chronic HAs. (18)
• Current research: identified polymorphisms in genes assoc w/ serotonergic, dopaminergic, and catecholaminergic systems in pts w/ FM. (19)
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Complex Etiology: Environmental triggers
Stressors involving: (1)
• acute pain
• motor vehicle traumas
• deployment to war
• infectious diseases
• psychological stress
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Pathophysiology and Pathogenesis
• Hallmark of FM = Centralized Pain • Process: CNS amplifies sensory input across many organ systems(20-21)
• But... can’t r/o peripheral nociceptive input as a contributing factor (22-23)
• Patients will respond with pain to presence of touch or light pressure (i.e. allodynia), or even from normal noxious stimluli (i.e. hyperalgesia)
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Pathophysiology and Pathogenesis 15
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Pathophysiology and Pathogenesis 16
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Pathophysiology and Pathogenesis
Central Sensitization
• A-delta fibers (large myelinated nociceptors) • transitory pain, easier to endure
• C-fibers (small unmyelinated nociceptors; free nerve endings) • chronic pain, harder to endure
• most numerous of sensory receptors and nociceptors
• bombardment of C-fibers in spinal cord proposed MOA FM central sensitization syndromes (chronically maintained and sympathetically maintained pain syndromes)
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Pathophysiology and Pathogenesis
Central Sensitization: BOMBARDMENT OF C-FIBERS
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• Required to processes influx of C-fibers
• Sprouting occurs (anatomic disorganized change in laminae)
Incr in NMDA receptors + glutamate
• Travels down peripheral receptors
• Ends at termination of C-fibers Incr Substance P production
• Incr receptor field in periphery
• Here: receptors more sensitive and more likely to depolarize “Wind Up”
Lowers
threshold
of C-fibers
Disorganizes
processing
of pain
Widened
receptor field
allows for A +
B to occur
A
B
C
C-fibers fire into IML Follow SNS
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Pathophysiology and Pathogenesis
• fMRI studies: (27,28)
• Pain when stimulated by mild pressure or a heat stimulus
• Pain assoc w/activation in brain areas involved in pain processing
• Decr cortical thickness in the DLPFC, anterior insula, anterior cingulate cortex and somatosensory cortex (SI, SII) (35)
19
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Pathophysiology and Pathogenesis 20
• Increased brain connectivity:
areas of increased pain
processing
• Decreased brain connectivity:
areas that attenuate pain
fRMI studies: (34)
Incr intrinsic DMN activity within
R. middle and ant. insula
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Pathophysiology and Pathogenesis
• Proton spectroscopy studies: (29-32)
• Increases and decreases in neuromodulators of pain
• Tx for FM: alter these by targeting their receptors
21
Figure 1: CNS neurotransmission influencing pain (34)
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Pathophysiology and Pathogenesis
• PET imaging studies: (44,45)
• Paradoxical incr in endogenous opioid activity and a decr in mu-opioid receptor availability
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Pathophysiology and Pathogenesis
• Glial cell activation and central inflammation • modulate pain by:
• (1) harboring neurotransmitter receptors
• (2) releasing neuromodulators in response to pain
23
Acute effects:
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Pathophysiology and Pathogenesis
• Glial cell activation and central inflammation • When chronically activated:
• pro-inflammatory cascade neurotoxicity
• ? explanation for central inflammatory process also involved in pathogenesis
• Glial cell modulating therapy:
• LDN
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Chronic effects:
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Pathophysiology and Pathogenesis
• Small fiber neuropathy • Defined: injury to peripheral nerves affecting small fibers
• Sx: burning, shooting, allodynia, hyperesthesia
• 2013 case-controlled study (46)
• FM pts: reduction in intraepidermal innervation and regeneration of C fibers
• Pts showed neuropathic pain
• Findings differed from healthy controls and unipolar depression w/o pain
• 2015 Retospective study (47)
• FM vs SFN and controls
• using EM: reduced axonal diameters of C-fibers (absent in SFN)
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Distal nerve
pathology in
FM?
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Pathophysiology and Pathogenesis
• SFN • Better hypothesis based on CNS theory (central sensitization):
• peripheral abnormalities d/t neuroplasticity or other co-morbid changes in chronic pain (e.g. deconditioning)?
• just a sequela of the syndrome?
• incidental finding?
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Pathophysiology and Pathogenesis
• Raymond Perrin, DO, PhD • Hypothesis:
• insulin – biofeedback w/hypothalamus; HPA disrupted insulin fx disrupted
• poor filtering/drainage of CSF in BOTH head and spine toxins build up in CSF d/t lymph backflow
• Common findings seen clinically
• Treatment: massage, OMT
• Anecdotally tx worked, confirmed findings in Journal of medical engineering and technology
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Pathophysiology and Pathogenesis 28
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Osteopathic Perspective
5 Domains of Pathology in FM
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Diagnosis
• Clinical Manifestation7: • Multifocal pain with low suspicion for a single etiology
• Amplified pain in other areas, usually earlier in life
• Symptoms suggestive of CNS origins
• Symptoms suggestive of global sensory hyper-responsiveness
• Pertinent past med hx:
• Co-morbid: chronic regional pain syndromes, rheumatic disease, psych
• Fam h/o FM
• Patient Self-Report Survey based on 2011 ACR Criteria Helpful for diagnosis
• Score of >/= 13 is consistent with FM.
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Diagnosis: ACR 2011 modified fibromyalgia criteria(7) 31
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Diagnosis: ACR 2011 modified fibromyalgia criteria(7) 32
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Diagnosis
• Physical Exam Findings • Diffuse tenderness assessed by
tenderpoint exam
• Blood pressure cuff sensitivity from insufflation
• Low pain threshold to firm pressure of upper extremities
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Diagnosis
• Perrin’s Signs: • head forward posture
• hyper mobility in cervical and lumbar region
• commonly thoracic problems
• incr in thoracic kyphosis and lordosis (T1-L2), mechanically SNS is over-irritated —> symptoms
• lymphatic varicosity
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Diagnosis 35
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Diagnosis 36
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Diagnosis 37
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Diagnosis 38
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Diagnosis
• Perrin’s Symptoms: • “Perrin’s points” - tender
points (stars in image)
• Tenderness at celiac plexus
• Abnml Cranial Rhythm
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Diagnosis
• “Fibro Fog” • Complaint: “I feel like I’ve been taking cold medicine
constantly”
• Symptoms: difficulty concentrating, finding words, holding conversations, feeling alert and remembering things
• Pathophysiology: (43)
1. Central processing abnormalities?
2. Morphologic abnormalities in the frontoparietal network?
3. Dysfunctional dopamine system?
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Diagnosis
• “Fibro Fog” • Diagnosis: (43)
• Neurocognitive testing (1) effects of distraction on memory (2) speed of word retrieval
• Treatment: (43)
• Acknowledge its existence and reassure
• Co-occurence of ADHD (inattentive) and fibro is high common neurobiology and ?rationale for stimulants ongoing open-label trials (methylphenidate 10-60mg)
• Better sleep (FM often have insomnia)
• Best option thus far: CBT+physical activity+meds
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Diagnosis
• Laboratory Tests • Blood Tests
• Results: non-specific
• If low suspicion for other causes: CBC, CMP, TSH, Vitamin D, ESR, and/or CRP.
• Rheum labs: (only if necessary): ANA and Rheumatoid factor.
• Ancillary Test
• Pts w/neuropathic signs (e.g. from SFN), or to r/o other causes: ENFD testing with skin punch biopsies
• Further W/U
• Imaging studies, muscle biopsies, EMGs, and mm enzyme assays
• Not required
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Differential
• Somatic Symptom Disorder (SSD), specifier: with predominant pain (DSM-V) • Previously: Somatoform Disorders (DSM-IV)
• Myofascial Pain Disorder
• Inflammatory Myopathies
• Polymyalgia Rheumatica
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Differential: SSD
Changes in new DSM-5: • Removal of DSM-IV disorders:
• somatization d/o, hypochondriasis, pain d/o, undifferentiated somatiform d/o many can now be diagnosed under SSD
• Somatization d/o required specific number of complaints from among 4 symptom groups
• SSD no longer requires this
• SSD does not require the presence of “medically unexplained symptoms” as an inclusion criteria
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Differential
• CFS/ME • controversial: unique or on spectrum?
• overlap with FM: sleep, mood, pain, fatigue
• Differences:
• CFS/ME fatigue primary c/o
• FM pain primary c/o
• Tx:
• same for both
• so... doesn’t matter what you call it
• Dr. Perrin and OMT
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Diagnosis: FM vs SSD
• It is difficult to differentiate the two b/c of similarities
• See functional somatic illnesses elsewhere in medicine, w/ overlapping sx and tx (CBT and meds) • Rheumatology: Fibromyalgia
• Infectious disease: Chronic fatigue syndrome
• Gastroenterology: Irritable bowel syndrome
• Neurology: Chronic headaches
• Cardiology: Noncardiac chest pain
• Urology: irritable bladder syndrome
• Gynecology: Vulvodynia and chronic pelvic pain
• Allergy: Multiple chemical sensitivity
• Oral surgeons: Temporomandibular joint syndrome
• Physical medicine: Myofascial pain syndrome
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Diagnosis: FM vs SSD
• Result of confusion? • Skepticism among the medical community that FM as a disease, truly exists
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Diagnosis: FM vs SSD
• What we know today: • FM is NOT SSD
• Need to establish diagnosis of FM – essential to tx (17)
• Key clinical differences to remember: • Pts usually do not focus on their condition to the exclusion of other life
interests, should not have markedly diminished social, sexual, and vocational functioning, and should not be profoundly physically deconditioned
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Diagnosis: FM vs SSD
• Result of incorrect dx: • Categorizing as having only SSD psychiatrization (25)
• Conversely, treating a patient for only FM pain ignoring sx of SSD and other psych factors poorer outcomes
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Diagnosis: Solution
• A more nuanced method: • use a multidimensional approach:
• patient’s somatic, psychosocial, and functional status
• categorizing on a spectrum of severity (e.g. mild to moderate) along with co-morbidities (e.g. FM plus IBS) to individualize treatment (25)
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Proposed method for diagnosing FM
Suspected FM begin a trial of treatment while evaluation of other co-morbidities (24)
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CCF Program Model
Established FM diagnosis
Individualized treatments
(psychology/PT)
6 week FM Psychology Group +/- PT Group
(mild-moderate symptoms)
Monthly Relapse Prevention Group
CPRP (moderate-severe symptoms)
One Day Program (mild-moderate
symptoms)
Initial Assessment (Rheum or NCP)
Directing Treatment
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Courtesy of Sara Davin, Psy.D, MPH
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Chronic Pain Rehabilitation and FM
• Admission: • Pain: moderate-severe • Functional impairment: severe • Depression: moderate • Anxiety: severe
• Discharge: • Pain: mild-moderate • Functional impairment: moderate • Normalization of anxiety/depression • Improvements were clinically and statistically significant (p < .01)
Vij et al. Poster at American Pain Society (2014)
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Courtesy of Sara Davin, Psy.D, MPH
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Do improvements last?
12 month follow-up
• 27.32% (n = 100) returned follow up surveys
• Pain: moderate
• Functional impairment: moderate
• Depression: moderate
• Anxiety: mild
• In comparison to admission, improvements remained clinically and statistically relevant (p < .01)
Vij et al. Poster to be presented at American Pain Society (2014)
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Treatment
• No treatment alters pathogenesis of disease
• Focus on symptoms relief and functional restoration
Conservative Management
Oral pharmacotherapy
Non-invasive treatments
Invasive treatments
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Treatment: Conservative Management
• *Patient education • Confirm FM label -- NO judgement
• Emphasize multimodal tx + active patient involvement
• *CBT • Pain based CBT in 1-1 sessions, groups, or via telemedicine
• *Graded Exercise • Aerobic exercise, strength training, stretching
• Nutrition • Weight loss (for those overweight or obese)
• Complementary medicine • Music: specifically water and wave sounds
• Other: Yoga, acupuncture, tai chi, chiropractic manipulation, myofascial release therapy, and osteopathic manipulation
* 3 best studies non-pharm tx for FM
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Components of CBT-based Skill Building
• Education
• Coping skills
• Activity pacing
• Problem solving skills
• Assertiveness training
• Emotional modulation
• Relaxation training
• Sleep hygiene
• Relapse prevention
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Treatment: Oral pharmacotherapy
Overarching goal of oral pharmacotherapy:
excitatory neurotransmission via:
inhibitory neurotransmission via:
58
glutamate,
substance P, and
nerve growth
factor activity
norepinephrine,
dopamine, and
GABA activity
Facilitate pain transmission
Inhibit pain transmission
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Treatment: Oral pharmacotherapy 59
Figure 1: CNS neurotransmission influencing pain (34)
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Treatment: Oral pharmacotherapy
TCAs and
SNRIs
•Amitriptyline: 10-70mg qhs
Cyclobenzaprine: 5-20mg qhs
•Duloxetine: 30-120mg qd (FDA approved)
Milnacipran: 100-200mg qd (FDA approved)
Venlafaxine XR: 75-225mg qd
Gabapentinoids and
GABA agents
•Gabapentin: up to 3600mg qd in divided doses
•Pregabalin: up to 600mg qd in divided doses (FDA approved)
•Gamma-hydroxybutyrate (sodium oxybate): 4.5-6.0 mg qd in divided doses
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First line – Level 1A
evidence
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Treatment: Oral pharmacotherapy
SSRIs • Fluoxetine
• Sertraline
• Paroxetine
Cyclobenzaprine
• Monotherapy: 10-40mg qd
• Combination: cyclobenzaprine 10mg qd + fluoxetine 20mg qd
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Second line –
no convincing
evidence
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Treatment: Oral pharmacotherapy
Opioids (full and weak opioid agonist): • History:
• Nidus: very poor 1986 retrospective review of 38 pts
• Fact:
• poor outcomes not recommended
• Unfortunately
• (1) use in FM is widespread, (2) those given opioids were unlikely to receive evidence based pharmacotherapy,(3) less likely to respond well opioids (41-42)
• Interestingly:
• patients have elevated CSF levels of endogenous opioids (38) + decreased binding capacity to mu-opioid receptors in pain areas of brain (39) ? account for poor outcomes (40)
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Treatment: Oral pharmacotherapy
• Low dose naltrexone: 4.5mg qhs (36)
• Promise in treating chronic pain conditions that involve inflammatory processes but FM doesn’t have inflammation in FM??
• Rationale: FM may involve chronic glial activation and subsequent production of pro-inflammatory cytokines
• Benefits: low SE profile, no abuse potential, low cost (on avg, $35/month vs >$100/month for conventional oral meds)
• Synthetic Cannabinoids (37)
• Nabilone: 0.5mg qhs to 1.0mg bid
• Limited available data with studies showing a non-significant trend for analgesia, but they may be a consideration in those with significant sleep disturbances
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Future treatment options: promising results, but lack sufficient data
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Treatment: Other treatments
• Non-invasive: • rTMS
• rTDCS and HD-rTDCS
• Hyperbaric O2 (prelim study)
• TENS unit (mixed results)?
• OMT and Soft Tissue Techniques
• Invasive:
• ONS
• TP injections?
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Treatment: Non-invasive treatments
• rTMS and HD-rTDCS • Target: left primary motor cortex and dorso-lateral
prefrontal cortex
• Study outcomes: (48,49)
• reduction in FM pain and effects outlasting the duration of stimulation
• outcomes similar to medications
• Benefits: minimal SE (most common: transient HA and scalp irritation)
• Studies: • on-going phase-II open label trial for HD-rTDCS (50)
• more targeted, more tolerable, higher specificity
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TD
CS
TM
S
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Treatment: Non-invasive treatments
• ESWT
• Concept: high energy acoustic waves (i.e. shock waves) delivers mechanical force
• Use: MSK pain (e.g. MPD)
• How it works in MPD (MOA still elusive)
• Shock waves elicit referred pain (from TPs) induces energy stimulates healing through inflammation and incr blood flow to damaged tissues promote healing
• In FM: (only 1 study to date) improvements 3-mo post tx, no SE (51)
• improved: VAS and algometer
• 2000 pulses in 5 sessions
• ?effective adjunct early in d/o
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Treatment: Invasive treatments
• ONS
• Use: migraine headaches, chronic primary HAs
• MOA: unclear
• SE: high risk of complications d/t invasive
• 2007 study (lacked placebo; co-morbid chronic HAs) (52)
• C2 scalp area; VAS , BDI, QOL (SF-36)
• HAs, widespread bodily pain, mood, and fatigue improved
• 2013 study (double-blind, placebo controlled) (53)
• subsensory threshold stimulation
• psych d/o excluded (except mild depression), no HAs, intractable to PT, meds, psych therapy
• decr (40-60%) in pain 6 mo post-implant (VAS and PCS, not BDI), decr in tender points
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Treatment: Perrin’s Plan
• cranial massage
• stimulating blood blood flow in shoulders with cold and heat
• draining motion down nose
• working fingers up chest
• rotating body around upper waist
• rotating shoulders
• marching up and down, shaking arms back and forth
• avoid stimulants - coffee and etoh
• watch for bad posture
• keeping spine straight while sleeping; pillow between knees
• proper sleep
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Treatment: Perrin’s Plan 69
• Video excerpt
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Treatment: OMT Overview
• Counterstrain of various bilateral tenderpoints assoc w/FM
• Rib raising
• Myofascial Release
• Muscle energy
• Balance Ligamentous Tension
• Facilitated Positional Release
• TMJ treatments
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Treatment: OMT Specifics
• Seated lumbosacral functional technique
• Seated lumbosacral functional technique
• Sidelying rib functional technique
• Seated upper thoracic spine muscle energy technique
• Seated or supine diaphragm myofascial release technique
• Supine cervical functional and strain/counterstrain techniques
• Supine TMJ muscle energy techniques
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Take Home Points
• FM-like symptoms described in texts dating back 100s of years
• First given a name in the 1600’s; 2007 FDA approved 1st drug
• Very common in rheum practices
• Onset between 35-55yo
• Symptoms increase with age, but see in children also
• Life long sx – mimic other pain d/o
• Defined on a spectrum of central sensitization d/o
• Active research - glial cell activation, central inflammation, and small fiber neuropathy, LDN, TMS, TDCS, ECWT, ONS
• Many options for management
• Left untreated – devastating for pt, provider and health care system
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References
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3. VincentA,LahrBD,WolfeF,etal.Prevalenceof fibromyalgia: a population-based study in Olmsted County, Minnesota, utilizing the Rochester Epidemiology Project. Arthritis Care Res (Hoboken). 2013;65(5):786-792.
4. Blanco I, Beritze N, Arguelles M, Carcaba V, Fernandez F, Janciauskiene S, Oikonomopoulou K, de Serres FJ, Fernandez-Bustillo E and Hollenberg MD (2010) Abnormal overexpression of mastocytes in skin biopsies of fibromyalgia patients. Clin Rheumatol 29:1403-1412.
5. Luo X, Cappelleri JC, Chandran A. The burden of fibromyalgia: assessment of health status using the EuroQol (EQ-5D) in patients with fibromyalgia relative to other chronic conditions. Health Outcomes Res Med. 2011;2(4):e203–e214
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9. Jain AK, Carruthers BM, van de Sande MI et al. (2003). Fibromyalgia syndrome: Canadian clinical working case definition, diagnostic and treatment protocols – a consensus document. J Musculoskelet Pain 11: 3–107.
10. Buskila D (2009). Pediatric fibromyalgia. Rheum Dis Clin North Am 35: 253–261
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12. Holliday KL, McBeth J. Recent advances in the understanding of genetic susceptibility to chronic pain and somatic symptoms. Curr Rheumatol Rep. 2011;13(6):521-527.
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15. Arnold LM, Hudson JI, Hess EV et al. (2004a). Family study of fibromyalgia. Arthritis Rheum 50: 944–952 Arnold LM, Hudson JI, Hess EV et al. (2004a). Family study of fibromyalgia. Arthritis Rheum 50: 944–952
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17. Hughes G, Martinez C, Myon E, et al. The impact of a diagnosis of fibromyalgia on health care resource use by primary care patients in the UK: an observational study based on clinical practice. Arthritis Rheum 2006; 54:177
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19. Park DJ, Kang JH, Yim YR, Kim JE, Lee JW, Lee KE, Wen L, Kim TJ, Park YW, Lee SS. Exploring Genetic Susceptibility to Fibromyalgia. Chonnam Med J. 2015 Aug;51(2):58-65. doi: 10.4068/cmj.2015.51.2.58. Epub 2015 Aug 17. Review. PubMed PMID: 26306300; PubMed Central PMCID: PMC4543151
20. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011;152(3 Suppl):S2-15
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References
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23. TraceyI,BushnellMC.Howneuroimaging studies have challenged us to rethink: is chronic pain a disease? J Pain. 2009;10(11):1113-1120
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25. King, S.A. (2013). The new somatic symptom disorder in DSM-5 risks mislabeling many people as mentally ill. BMJ 346, f1580
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27. Gracely RH, Petzke F, Wolf JM, Clauw DJ. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum. 2002;46(5):1333-1343
28. Cook DB, Lange G, Ciccone DS, Liu WC, Steffener J, Natelson BH. Functional imaging of pain in patients with primary fibromyalgia. J Rheumatol. 2004;31(2):364-378
29. Napadow V, LaCount L, Park K, As-Sanie S, Clauw DJ, Harris RE. Intrinsic brain connectivity in fibromyalgia is associated with chronic pain intensity. Arthritis Rheum. 2010;62(8): 2545-2555
30. Napadow V, Kim J, Clauw DJ, Harris RE. Decreased intrinsic brain connectivity is associated with reduced clinical pain in fibromyalgia. Arthritis Rheum. 2012;64(7):2398-2403
31. Jensen KB, Loitoile R, Kosek E, et al. Patients with fibromyalgia display less functional connectivity in the brain’s pain inhibitory network. Mol Pain. 2012;8:32
32. Jensen KB, Kosek E, Petzke F, et al. Evidence of dysfunctional pain inhibition in fibromyalgia reflected in rACC during provoked pain. Pain. 2009;144(1-2):95-100
33. Goksan S, Hartley C, Emery F, Cockrill N, Poorun R, Moultrie F, Rogers R, Campbell J, Sanders M, Adams E, Clare S, Jenkinson M, Tracey I, Slater R. fMRI reveals neural activity overlap between adult and infant pain. Elife. 2015 Apr 21;4.
34. Clauw DJ. Fibromyalgia and related conditions. Mayo Clin Proc. 2015 May;90(5):680-92. doi: 10.1016/j.mayocp.2015.03.014. Review. PubMed PMID: 25939940
35. Seminowicz DA, Wideman TH, Naso L, Hatami-Khoroushahi Z, Fallatah S, Ware MA, Jarzem P, Bushnell C, Shir Y, Ouellet JA (2011) Effective Treatment of Chronic Low Back Pain in Humans Reverses Abnormal Brain Anatomy and Function. The Journal of Neuroscience 31(20): 7540-755
36. Younger J, Mackey S. Fibromyalgia symptoms are reduced by low- dose naltrexone: a pilot study. Pain Med. 2009;10(4):663-672
37. Calandre EP, Rico-Villademoros F, Slim M. An update on pharmacotherapy for the treatment of fibromyalgia. Expert Opin Pharmacother. 2015 Jun;16(9):1347-68. doi: 10.1517/14656566.2015.1047343. Review. PubMed PMID: 26001183
38. Schweinhardt P, Sauro KM, Bushnell C (2008). Fibromyalgia: a disorder of the brain? Neuroscientist 14: 415–421
39. Harris RE, Clauw DJ, Scott DJ et al. (2007). Decreased central mu-opioid receptor availability in fibromyalgia. J Neurosci 27: 10000–10006
40. Arnold LM (2009). Strategies for managing fibromyalgia. Am J Med 122: S31–S43
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References
41. Halpern R, Shah SN, Cappelleri JC, Masters ET, Clair A. Evaluating Guideline-recommended Pain Medication Use Among Patients with Newly Diagnosed Fibromyalgia. Pain Pract. 2015 Oct 7. doi: 10.1111/papr.12364. [Epub ahead of print] PubMed PMID: 26443495
42. BrummettCM,JandaAM,SchuellerCM,etal. Survey criteria for fibromyalgia independently predict increased postoperative opioid consumption after lower-extremity joint arthroplasty: a prospective, observational cohort study. Anesthesiology. 2013;119(6):1434-1443
43. Kravitz HM, Katz RS. Fibrofog and fibromyalgia: a narrative review and implications for clinical practice. Rheumatol Int. 2015 Jul;35(7):1115-25.
44. Wood PB, Schweinhardt P, Jaeger E, et al. Fibromyalgia patients show an abnormal dopamine response to pain. Eur J Neurosci. 2007;25(12):3576-3582
45. Harris RE, Clauw DJ, Scott DJ, McLean SA, Gracely RH, Zubieta JK. Decreased central mu-opioid receptor availability in fibromyalgia. J Neurosci. 2007;27(37):10000-10006
46. Üçeyler N, Zeller D, Kahn AK, Kewenig S, Kittel-Schneider S, Schmid A, Casanova-Molla J, Reiners K, Sommer C. Small fibre pathology in patients with fibromyalgia syndrome. Brain. 2013 Jun;136(Pt 6):1857-67. doi: 10.1093/brain/awt053. Epub 2013 Mar 9. PubMed PMID: 23474848
47. Clauw DJ. What is the meaning of "small fiber neuropathy" in fibromyalgia? Pain. 2015 Nov;156(11):2115-6. doi: 10.1097/j.pain.0000000000000311. PubMed PMID: 26307862.
48. Young NA, Sharma M, Deogaonkar M. Transcranial magnetic stimulation for chronic pain. Neurosurg Clin N Am. 2014 Oct;25(4):819-32. doi: 10.1016/j.nec.2014.07.007. Epub 2014 Aug 12. Review. PubMed PMID: 25240669
49. Marlow NM, Bonilha HS, Short EB. Efficacy of transcranial direct current stimulation and repetitive transcranial magnetic stimulation for treating fibromyalgia syndrome: a systematic review. Pain Pract. 2013 Feb;13(2):131-45. doi: 10.1111/j.1533-2500.2012.00562.x. Epub 2012 May 28. Review. PubMed PMID: 22631436
50. Castillo Saavedra L, Gebodh N, Bikson M, Diaz-Cruz C, Brandao R, Coutinho L, Truong D, Datta A, Shani-Hershkovich R, Weiss M, Laufer I, Reches A, Peremen Z, Geva A, Parra LC, Fregni F. Clinically effective treatment of fibromyalgia pain with HD-tDCS - Phase II open-label dose-optimization. J Pain. 2015 Oct 5. pii: S1526-5900(15)00884-6. doi: 10.1016/j.jpain.2015.09.009. [Epub ahead of print] PubMed PMID: 26456677
51. Ramon S, Gleitz M, Hernandez L, Romero LD. Update on the efficacy of extracorporeal shockwave treatment for myofascial pain syndrome and fibromyalgia. Int J Surg. 2015 Sep 10. pii: S1743-9191(15)01195-4. doi: 10.1016/j.ijsu.2015.08.083. [Epub ahead of print] Review. PubMed PMID: 26363497
52. Thimineur M, De Ridder D. C2 area neurostimulation: a surgical treatment for fibromyalgia. Pain Med 2007;8:639–646
53. Plazier M, Dekelver I, Vanneste S, Stassijns G, Menovsky T, Thimineur M, De Ridder D. Occipital nerve stimulation in fibromyalgia: a double-blind placebo-controlled pilot study with a six-month follow-up. Neuromodulation. 2014 Apr;17(3):256-63; discussion 263-4.
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References: OMM
• Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum 2008;58(1):26–35.
• Smith HS, Harris R, Clauw D. Fibromyalgia: an afferent processing disorder leading to a complex pain generalized syndrome. Pain Physician 2011;14 (2):E217-45.
• Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the multicenter criteria committee. Arthritis Rheum 1990; 33:160–72.
• www.uptodate.com.arktos.nyit.edu/contents/clinical-manifestations-and-diagnosis-of- fibromyalgia-in-adults?source=search_result&search=fibromyalgia&selectedTitle=2%7E127
• www.uptodate.com.arktos.nyit.edu/contents/initial-treatment-of-fibromyalgia-in- adults?source=search_result&search=fibromyalgia&selectedTitle=3%7E127
• Gamber R., Shores J., Russo D., Jimenez C., Rubin B. Osteopathic manipulative treatment in conjunction with medication relieves pain associated with fibromyalgia syndrome: Results of a randomized clinical pilot project. JAOA 2002; Vol 102: No 6. —> This study found OMT combined with standard medical care was more efficacious in treating FM than standard care alone.
• Seffinger M. Osteopathic Approach to the Patient with Fibromyalgia. American Osteopathic Association Annual Scientific Convention and Medical Education Conference. 2010
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Online Resources*
• http://www.niams.nih.gov/Health_Info/Fibromyalgia/fibromyalgia_ff.asp
• http://www.mayoclinic.org/diseases-conditions/fibromyalgia/in-depth/fibromyalgia/art-20048097
• https://my.clevelandclinic.org/health/diseases_conditions/hic_Fibromyalgia
• http://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions/Fibromyalgia
• http://www.fmaware.org/about-fibromyalgia/
*Accessed 02/04/2017
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