Fibromyalgia — Med2Date

📋 Key Information Summary

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Fibromyalgia is a central sensitisation syndrome characterised by chronic widespread pain (CWP), fatigue, sleep disturbance, and cognitive dysfunction — diagnosis is clinical, supported by the 2016 ACR Preliminary Diagnostic Criteria.
The 2016 ACR criteria use the Widespread Pain Index (WPI) and Symptom Severity Scale (SSS); generalised pain in ≥4 of 5 body regions plus SSS ≥9 (or WPI 4–6 + SSS ≥12) meets the threshold, with symptoms present ≥3 months.
Chronic widespread pain is the hallmark feature — must be present for ≥3 months, typically bilateral, above and below the waist, and involving the axial skeleton.
Fatigue and non-restorative sleep are near-universal; poor sleep quality amplifies pain perception and functional impairment.
"Fibro fog" (cognitive dysfunction) affects concentration, working memory, and multitasking; it is an independent driver of disability and reduced quality of life.
Non-pharmacological therapy is first-line: graded exercise therapy (GET) and cognitive behavioural therapy (CBT) have the strongest evidence base and should be initiated before or alongside pharmacotherapy.
Three medications are PBS-listed for fibromyalgia in Australia — amitriptyline (low-dose), duloxetine (SNRI), and pregabalin (α2δ ligand) — all considered first-line pharmacological options.
Amitriptyline 10–25 mg nocte is a well-established, inexpensive first-line option; titrate cautiously to 50 mg if tolerated; anticholinergic side effects limit dose escalation.
Duloxetine 60 mg daily (range 30–120 mg) is effective for pain, fatigue, and comorbid depression/anxiety; PBS Authority Required for fibromyalgia.
Pregabalin 150–450 mg/day in divided doses reduces pain and improves sleep; dose-reduce in renal impairment (eGFR <60); PBS Authority Required for fibromyalgia.
Opioids, benzodiazepines, and NSAIDs as monotherapy are NOT recommended — they lack efficacy in central sensitisation pain and carry significant harm.
ATSI Australians have higher prevalence of chronic pain and CWP; culturally safe, multidisciplinary care and remote-access strategies are essential.
Comorbid anxiety, depression, and irritable bowel syndrome are common; a biopsychosocial approach addressing all domains improves outcomes.
Diagnosis should exclude inflammatory rheumatological disease, hypothyroidism, and other causes of widespread pain — but avoid excessive investigation once red flags are excluded.
Shared decision-making, patient education about central sensitisation, and realistic goal-setting are foundational to successful management.

Introduction & Australian Epidemiology

Fibromyalgia is a chronic, centralised pain syndrome characterised by widespread musculoskeletal pain accompanied by fatigue, sleep disturbance, memory difficulties, and mood disturbance. It is classified among the central sensitisation syndromes and represents a disorder of pain processing rather than peripheral tissue damage.

In Australia, the prevalence of fibromyalgia is estimated at 2–5% of the adult population, with a female-to-male ratio of approximately 3:1. The condition is seen across all age groups but most commonly presents between ages 30 and 60 years. The Australian Institute of Health and Welfare (AIHW) identifies chronic widespread pain as a significant contributor to disability and healthcare utilisation.

Fibromyalgia frequently coexists with other conditions including irritable bowel syndrome (IBS), temporomandibular joint disorder, tension-type headache, migraine, interstitial cystitis, chronic fatigue syndrome, depression, and anxiety. The biopsychosocial model is the accepted framework for understanding and managing fibromyalgia in Australian practice.

The economic burden is substantial, with significant costs relating to healthcare visits, medications, lost productivity, and disability payments. Early recognition and evidence-based management can reduce this burden and improve patient outcomes.

2016 ACR Diagnostic Criteria

The 2016 Revisions to the 2010 American College of Rheumatology (ACR) Preliminary Diagnostic Criteria for Fibromyalgia are the current standard for clinical diagnosis. These criteria replaced the 1990 tender-point examination and can be applied in both clinical and research settings.

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Diagnostic requirements — all four must be met:

Generalised pain defined as pain in ≥4 of 5 body regions (left upper, right upper, left lower, right lower, axial) — jaw, chest, and abdominal pain may be included.
Symptoms present at a similar level for ≥3 months.
Widespread Pain Index (WPI) ≥7 and Symptom Severity Scale (SSS) ≥5, OR WPI 4–6 and SSS ≥9.
A diagnosis of fibromyalgia is valid irrespective of other diagnoses; it does not exclude the presence of other clinically important illnesses.

Widespread Pain Index (WPI)

The patient identifies areas of pain in the prior week from a list of 19 body areas. Score 0–19.

Body Region	Areas Scored
Left upper	Shoulder girdle, upper arm, lower arm
Right upper	Shoulder girdle, upper arm, lower arm
Left lower	Hip, upper leg, lower leg
Right lower	Hip, upper leg, lower leg
Axial	Jaw (L & R), upper back, lower back, chest, abdomen, neck

Symptom Severity Scale (SSS)

Rate each of three symptoms (fatigue, waking unrefreshed, cognitive symptoms) on a 0–3 scale (0 = no problem, 3 = severe, pervasive, continuous, life-disturbing). Add the score of somatic symptoms in general (0–3). Total score range: 0–12.

2016 Revisions — Key Changes

The requirement for a separate clinical diagnosis of fibromyalgia by a physician was removed — self-report and physician-applied criteria are equivalent.
The term "generalised pain" replaced the earlier descriptor to allow inclusion of jaw, chest, and abdominal pain.
The criteria acknowledge that fibromyalgia can coexist with other rheumatic and non-rheumatic conditions — it is not a diagnosis of exclusion.
The polysymptomatic distress scale (PSD = WPI + SSS, range 0–31) can track disease severity longitudinally.

Differential Diagnoses to Exclude

Before confirming fibromyalgia, the following should be considered and excluded where clinically appropriate:

Inflammatory rheumatic diseases — rheumatoid arthritis, systemic lupus erythematosus, polymyalgia rheumatica, spondyloarthropathy
Endocrine disorders — hypothyroidism, hyperparathyroidism, acromegaly, Cushing syndrome
Neurological conditions — multiple sclerosis, myasthenia gravis, small fibre neuropathy
Infections — hepatitis C, HIV, Lyme disease (rare in Australia)
Medications — statins, aromatase inhibitors, proton pump inhibitors
Vitamin D deficiency, iron deficiency, and obstructive sleep apnoea should be assessed

Chronic Widespread Pain

Chronic widespread pain (CWP) is the cardinal symptom of fibromyalgia and the primary reason patients seek medical attention. It is defined as pain present for ≥3 months, affecting both sides of the body, above and below the waist, and involving the axial skeleton (cervical spine, anterior chest, thoracic spine, or low back).

Pathophysiology of Central Sensitisation

CWP in fibromyalgia results from amplified central nervous system pain processing — termed central sensitisation. Key mechanisms include:

Ascending facilitation: Increased excitability of dorsal horn neurons leads to wind-up and expanded receptive fields.
Descending inhibition failure: Reduced serotonergic and noradrenergic descending inhibitory pathways fail to modulate nociceptive input.
Neurochemical imbalance: Elevated substance P and glutamate in cerebrospinal fluid; reduced serotonin, norepinephrine, and dopamine.
Functional brain changes: fMRI studies demonstrate augmented pain-processing regions (insula, anterior cingulate cortex, somatosensory cortex) at equivalent stimulus intensity.
Small fibre neuropathy: Skin biopsy studies in a subset of patients show reduced intraepidermal nerve fibre density, suggesting peripheral contribution in some cases.

Clinical Features of CWP in Fibromyalgia

Pain is typically described as deep, aching, burning, or gnawing; may fluctuate in intensity
Exacerbated by stress, cold, poor sleep, physical inactivity, and hormonal changes
Allodynia (pain from normally non-painful stimuli) and hyperalgesia (amplified pain response) are common
Pain may migrate between regions; whole-body pain flares are characteristic
Comorbid regional pain syndromes (e.g., myofascial pain, tension headache) frequently overlap

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Australian context: The prevalence of CWP in Australia is approximately 10–15% of the general adult population, with fibromyalgia representing a subset meeting ACR criteria. Rural and remote Australians face additional barriers including limited access to rheumatology and pain medicine specialists.

Fatigue & Sleep Disturbance

Fatigue and sleep disturbance are core symptoms of fibromyalgia, present in >90% of patients. They are bidirectionally related to pain — poor sleep amplifies pain perception, and pain disrupts sleep architecture.

Fatigue

Fatigue in fibromyalgia is typically described as overwhelming, persistent, and disproportionate to exertion. It differs from normal tiredness in its persistence despite rest and its interference with daily function.

Present on waking and worsens throughout the day in many patients
May be exacerbated by physical activity, cognitive tasks, and emotional stress
Significantly impacts work capacity, social engagement, and quality of life
Contributes to deconditioning and social withdrawal if not addressed

Sleep Disturbance

Polysomnographic studies reveal characteristic sleep abnormalities in fibromyalgia:

Alpha-delta sleep: Intrusion of alpha-frequency (wake) waves into delta (deep) sleep — the most consistent polysomnographic finding
Reduced slow-wave (Stage N3) sleep and fragmented sleep architecture
Increased periodic limb movements of sleep (PLMS) and restless legs syndrome
Non-restorative sleep — patients wake feeling unrefreshed regardless of sleep duration
Comorbid obstructive sleep apnoea should be assessed, especially in patients with BMI ≥30 or significant snoring

Management of Fatigue and Sleep

Sleep hygiene education — consistent bedtime, dark/cool room, limit screens, avoid caffeine after midday
CBT for insomnia (CBT-I) — evidence-based, improves sleep quality and fatigue
Low-dose amitriptyline (10–25 mg nocte) improves sleep quality and reduces pain; anticholinergic effects may limit use
Pregabalin improves sleep architecture and reduces pain — useful when sleep disruption is prominent
Graded exercise therapy improves fatigue and sleep over time — even modest increases in activity are beneficial
Melatonin (2–3 mg nocte) may be trialled for circadian disturbance; limited evidence in fibromyalgia specifically

Cognitive Symptoms ("Fibro Fog")

Cognitive dysfunction, colloquially termed "fibro fog," is a well-recognised and often distressing feature of fibromyalgia. It is included in the 2016 ACR criteria as one of three SSS symptom domains.

Cognitive Domains Affected

Working memory: Difficulty holding information in mind (e.g., phone numbers, instructions)
Attention and concentration: Easily distracted, difficulty sustaining focus on tasks
Executive function: Impaired planning, multitasking, and decision-making
Verbal fluency: Word-finding difficulties, tip-of-the-tongue phenomena
Processing speed: Slower information processing, particularly under time pressure

Contributing Factors

Fibro fog is multifactorial and exacerbated by:

Sleep deprivation and non-restorative sleep
Chronic pain — attentional resources diverted to pain processing
Comorbid depression and anxiety
Medication side effects (opioids, benzodiazepines, first-generation antihistamines)
Physical deconditioning and reduced aerobic fitness

Management

Address underlying contributors — optimise sleep, treat depression/anxiety, review medications
CBT improves cognitive function indirectly through pain and mood improvement
Graded exercise improves cerebral perfusion and cognitive outcomes
Cognitive pacing — breaking tasks into manageable segments with rest breaks
Neuropsychological rehabilitation may benefit selected patients with significant impairment
Avoid opioids and benzodiazepines which worsen cognitive function

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Do not dismiss cognitive symptoms: Fibro fog is real, measurable, and profoundly disabling for many patients. Normal screening bloods and standard cognitive tests may not capture the deficit. Validate the patient's experience and focus on modifiable contributors.

Non-Pharmacological Therapy

Non-pharmacological therapy is the cornerstone of fibromyalgia management and should be first-line, initiated before or concurrently with pharmacotherapy. The strongest evidence supports graded exercise therapy and cognitive behavioural therapy.

Graded Exercise Therapy (GET)

Regular aerobic exercise is one of the most effective interventions for fibromyalgia, with benefits across pain, fatigue, sleep, and mood domains.

Start at low intensity (e.g., walking 10–15 minutes, 3 times/week) and gradually increase over weeks to months
Target: 150 minutes/week of moderate-intensity aerobic activity (e.g., brisk walking, swimming, cycling)
Aquatic exercise is particularly well-tolerated — warm water reduces pain and supports movement
Resistance training 2–3 times/week improves strength, function, and pain
Tai chi and yoga have moderate evidence for fibromyalgia — improve pain, sleep, and quality of life
Exercise should be self-paced and gradually progressed; avoid boom-bust cycles

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Exercise prescription — key message: The best exercise is the one the patient will do consistently. Collaborate with the patient to choose an activity they enjoy. A physiotherapist referral for a supervised graded programme improves adherence and outcomes. Medicare Chronic Disease Management (CDM) items (GPMP/TCA) support allied health access.

Cognitive Behavioural Therapy (CBT)

CBT is the psychological therapy with the strongest evidence base for fibromyalgia. It targets maladaptive pain cognitions, catastrophising, and avoidance behaviours.

Typically 6–12 sessions delivered by a psychologist experienced in chronic pain
Reduces pain intensity, improves function, and decreases healthcare utilisation
Addresses catastrophising, fear-avoidance, and pain self-efficacy
Acceptance and Commitment Therapy (ACT) is an emerging alternative with growing evidence
Telehealth delivery is effective and improves access for rural/remote patients
Medicare Better Access initiative provides up to 10 individual and 10 group sessions per year with a GP Mental Health Treatment Plan

Other Non-Pharmacological Approaches

Intervention	Evidence Level	Key Considerations
Patient education	Strong	Explanation of central sensitisation model; reduces catastrophising
Sleep hygiene / CBT-I	Strong	Improves sleep quality; reduces pain amplification
Multidisciplinary pain programme	Strong	Combines physiotherapy, psychology, occupational therapy
Acupuncture	Moderate	Short-term pain relief; may be trialled as adjunct
Mindfulness-based stress reduction	Moderate	Reduces pain catastrophising and improves coping
Hydrotherapy / balneotherapy	Moderate	Warm water exercise well-tolerated; improves pain and function

Australian Medicare Support

GP Management Plan (GPMP) — MBS Item 721: Enables up to 5 individual allied health services per calendar year
Team Care Arrangement (TCA) — MBS Item 723: Coordinates multidisciplinary care
Mental Health Treatment Plan — MBS Items 2700/2701: Up to 10 individual + 10 group psychology sessions per year
Chronic Disease Management: Reviews (MBS Item 732) at least every 12 months

Pharmacotherapy

Pharmacotherapy for fibromyalgia targets the central mechanisms of pain processing. In Australia, three medications have specific PBS listings for fibromyalgia: amitriptyline, duloxetine, and pregabalin. All are considered first-line, and the choice depends on the patient's symptom profile, comorbidities, and tolerability.

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Opioids, NSAIDs, and benzodiazepines are NOT recommended for fibromyalgia. There is no evidence of efficacy for opioids in central sensitisation pain; they carry risks of dependence, hyperalgesia, and cognitive impairment. NSAIDs lack efficacy as monotherapy. Benzodiazepines worsen fatigue and cognitive symptoms and carry dependence risk.

First-Line Pharmacotherapy

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Amitriptyline

Endep® · Generic · Tricyclic antidepressant (TCA)

Mechanism Inhibits serotonin and noradrenaline reuptake; enhances descending inhibitory pathways; improves sleep architecture

Adult dose Start 5–10 mg PO nocte; titrate to 25–50 mg nocte (max 75 mg nocte for pain)

Paediatric dose Limited evidence; specialist supervision required if considered in adolescents

Route & frequency Oral, once nightly, 1–2 hours before bed

Duration Trial ≥8–12 weeks before assessing efficacy; long-term use if beneficial

Renal adjustment No specific dose adjustment; use caution in severe impairment

Hepatic adjustment Reduce dose or avoid in significant hepatic impairment

Key side effects Dry mouth, drowsiness, weight gain, constipation, urinary retention, cardiac conduction changes (ECG if >50 mg or cardiac history)

PBS status ✔ PBS General Benefit

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Duloxetine

Cymbalta® · Irenka® · SNRI

Mechanism Serotonin-noradrenaline reuptake inhibitor; enhances descending pain inhibition; also effective for comorbid depression and anxiety

Adult dose Start 30 mg PO daily for 1–2 weeks; then 60 mg daily; range 60–120 mg/day

Paediatric dose Not established for fibromyalgia in children/adolescents

Route & frequency Oral, once daily (morning preferred to minimise insomnia)

Duration Trial ≥8–12 weeks; long-term maintenance if beneficial

Renal adjustment Avoid if CrCl <30 mL/min

Hepatic adjustment Avoid in significant hepatic impairment; reduce dose in mild-moderate

Key side effects Nausea (common, often transient), headache, dizziness, dry mouth, constipation, hyperhidrosis, elevated blood pressure

PBS status ⚡ PBS Authority Required

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Pregabalin

Lyrica® · Generic · α2δ ligand (gabapentinoid)

Mechanism Binds α2δ subunit of voltage-gated calcium channels; reduces excitatory neurotransmitter release; modulates central sensitisation

Adult dose Start 75 mg PO BD; titrate to 150–225 mg BD (max 450 mg/day); reduce if intolerable dizziness/somnolence

Paediatric dose Not established for fibromyalgia in children/adolescents

Route & frequency Oral, twice daily (morning and evening)

Duration Trial ≥8–12 weeks; long-term if beneficial; reassess periodically

Renal adjustment Mandatory dose reduction — CrCl 30–60: max 300 mg/day; CrCl 15–30: max 150 mg/day; CrCl <15: max 75 mg/day

Hepatic adjustment No specific adjustment (minimal hepatic metabolism)

Key side effects Dizziness, somnolence, weight gain, peripheral oedema, blurred vision; may cause dependence — taper to discontinue

PBS status ⚡ PBS Authority Required

Choosing First-Line Therapy

Clinical Scenario	Preferred Agent	Rationale
Pain + insomnia predominant	Amitriptyline	Improves sleep architecture; low cost (PBS General Benefit)
Pain + depression/anxiety	Duloxetine	Dual action on pain and mood; also licensed for GDD/MDD
Pain + prominent neuropathic features	Pregabalin	Effective for allodynia and hyperalgesia; improves sleep
Anticholinergic intolerance (elderly)	Duloxetine or Pregabalin	Avoid TCA side effects in older patients
Obesity / weight concerns	Duloxetine	Weight-neutral; amitriptyline and pregabalin associated with weight gain

Combination Therapy

If monotherapy provides inadequate response, combination of agents from different classes may be considered (e.g., amitriptyline + pregabalin, or duloxetine + pregabalin). Evidence is limited but supported by clinical practice. Avoid combining duloxetine and amitriptyline (serotonin syndrome risk — generally low but monitor).

Agents NOT Recommended / Limited Evidence

Agent	Recommendation	Rationale
Opioids (tramadol, oxycodone, codeine)	NOT recommended	No efficacy in central sensitisation; risk of dependence, hyperalgesia
NSAIDs	NOT as monotherapy	Lack central mechanism; may be adjunct for peripheral pain component
Benzodiazepines	NOT recommended	Worsen fatigue and cognition; dependence risk; no evidence
Gabapentin	Second-line / off-label	Less evidence than pregabalin; TID dosing; not PBS-listed for FM
Milnacipran	Not available in Australia	SNRI approved for FM overseas but not TGA-registered

Monitoring

Fibromyalgia is a chronic condition requiring longitudinal management with regular review and reassessment. A structured approach to monitoring improves outcomes and reduces polypharmacy.

Monitoring Framework

Baseline

Confirm diagnosis using 2016 ACR criteria; document WPI and SSS
Baseline bloods: FBC, EUC, LFT, TFT, HbA1c, ferritin, vitamin D, CRP/ESR
Assess comorbid depression/anxiety (PHQ-9, GAD-7); screen for sleep apnoea if indicated
Functional assessment and patient-defined goals
ECG if commencing amitriptyline >25 mg or cardiac history

4–6 weeks

Assess tolerability and side effects of pharmacotherapy
Titrate dose if tolerated and subtherapeutic
Review exercise adherence and CBT engagement

12 weeks

Formal efficacy assessment — pain (VAS/NRS), function, sleep, mood
If inadequate response: optimise dose, switch agent, or consider combination
Reassess PSD score (WPI + SSS) as longitudinal measure

6–12 monthly

Review ongoing need for medications; attempt dose reduction if stable
Reassess functional goals; adjust management plan
Screen for new comorbidities; review polypharmacy
GP Management Plan review (MBS Item 732)

Special Populations

🤰 Pregnancy

Amitriptyline: Category C. Use with caution; lowest effective dose. Limited data suggest low risk at low doses in second/third trimesters. Avoid in first trimester if possible.

Duloxetine: Category C. Avoid in third trimester (neonatal withdrawal syndrome). Discontinuation syndrome risk if ceased abruptly. Weigh risk-benefit carefully.

Pregabalin: Category B3. Limited human data; use only if benefits outweigh risks. Animal studies show developmental toxicity at high doses.

Preferred approach: Non-pharmacological strategies (graded exercise, sleep hygiene, CBT) are first-line in pregnancy. Paracetamol for acute flares.

👶 Paediatrics & Adolescents

Fibromyalgia (juvenile primary fibromyalgia syndrome) can occur in adolescents, more commonly in girls aged 13–18.

Diagnosis: Modified 2016 ACR criteria may be applied; WPI thresholds may need adjustment.

Management: Non-pharmacological therapy is strongly preferred — physiotherapy, graded exercise, psychological support (CBT), and school accommodations.

Pharmacotherapy: Limited evidence. Low-dose amitriptyline may be considered under specialist supervision. Pregabalin and duloxetine are not established in paediatric fibromyalgia.

👴 Elderly (≥65 years)

Amitriptyline: Use with extreme caution — anticholinergic burden increases fall risk, cognitive impairment, urinary retention, and cardiac arrhythmia. Consider alternatives.

Duloxetine: Preferred SNRI in elderly; monitor blood pressure; falls risk with dizziness.

Pregabalin: Start low (25–50 mg BD); assess renal function (eGFR declines with age); falls risk with dizziness and sedation.

General: Avoid polypharmacy; non-pharmacological strategies are essential; regular medication review.

🫘 Renal Impairment

Amitriptyline: No specific dose adjustment; metabolites accumulate — use lowest effective dose in severe CKD.

Duloxetine: Avoid if CrCl <30 mL/min. Use cautiously in moderate impairment.

Pregabalin: Mandatory dose adjustment — see pharmacotherapy section. Monitor for increased sedation and dizziness.

🫁 Hepatic Impairment

Amitriptyline: Hepatically metabolised — reduce dose in mild-moderate impairment; avoid in severe liver disease.

Duloxetine: Avoid in significant hepatic impairment (Child-Pugh B/C). Monitor LFTs if used.

Pregabalin: Minimal hepatic metabolism — preferred in hepatic impairment. No dose adjustment required.

🛡️ Immunocompromised

Fibromyalgia is not an immunological condition; immunosuppressive status does not directly alter management.

Be cautious of drug interactions with immunosuppressants — duloxetine has CYP2D6 interactions (e.g., with some chemotherapeutic agents).

Differentiate fibromyalgia pain from inflammatory/infectious causes in immunocompromised patients — lower threshold for investigation.

ATSI Health Considerations

Aboriginal and Torres Strait Islander Health

Prevalence & burden

Chronic widespread pain and musculoskeletal conditions are significantly more prevalent among Aboriginal and Torres Strait Islander Australians. AIHW data show that chronic pain affects ATSI populations at 1.5–2 times the rate of non-Indigenous Australians, with higher associated disability and reduced quality of life.

Access to specialist care

Rural and remote ATSI communities face severe shortages of rheumatologists, pain medicine specialists, psychologists, and physiotherapists. Telehealth (MBS items for ATSI patients) is a critical enabler for specialist consultation. Aboriginal Community Controlled Health Organisations (ACCHOs) should be engaged as the primary care hub.

Cultural safety

Diagnosis and management must be delivered in a culturally safe framework. Yarning-based consultations, family/carer involvement, and acknowledgement of social and emotional wellbeing concepts (connectedness to land, culture, spirituality, family, and community) are essential. Avoid dismissive approaches to pain reporting.

Psychosocial factors

Intergenerational trauma, socioeconomic disadvantage, housing insecurity, and food insecurity amplify chronic pain burden and reduce capacity for self-management strategies like exercise and dietary modification. Address social determinants alongside clinical management.

Medication access

PBS co-payments can be a barrier despite Closing the Gap PBS co-payment measure — ensure patients are registered. Remote pharmacy access may be limited; consider long-acting formulations and medication supply via Remote Area Aboriginal Health Services. Check for CTG eligibility (PBS co-payment exemption for eligible ATSI patients).

Non-pharmacological strategies

Adapt exercise programmes to local context — walking groups, community-based activity programmes, and culturally appropriate physical activities. Indigenous-specific allied health services and programmes (e.g., through ACCHOs) should be prioritised. Telehealth psychology services can supplement face-to-face care.

Comorbidity burden

Higher rates of diabetes, cardiovascular disease, renal disease, and mental health conditions in ATSI populations mean fibromyalgia management must be integrated within comprehensive chronic disease management. Duloxetine may be preferred when comorbid depression is significant; pregabalin dose adjustment is critical given higher CKD prevalence.

📚 References

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