Clinicians

Clinicians play a vital role in recognising, diagnosing, and supporting people living with Myalgic Encephalomyelitis (ME), Long COVID and co-existing long-term overlapping conditions. This section provides clear, evidence‑based information to help you navigate these complex conditions with confidence and compassion. Here, you’ll find up‑to‑date diagnostic criteria, clinical guidance, management approaches, and links to national and international standards. You can also access education modules, sector resources, and information about upcoming professional events and training opportunities. Whether you’re a GP, specialist, allied health professional, or part of the wider care team, this page is designed to support your practice and strengthen care for patients across Aotearoa.

1 Myalgic Encephalomyelitis (ME) and Long COVID	7 Historical Context: How ME was Misclassified as Psychological
2 Biomedical Mechanisms	8 Differential Diagnosis: Rule-outs and Multi-morbidities
3 Post-Viral Onset Patterns	9 Causes and Aetiology
4 Symptom Clusters	10 Genetic Predisposition and Risk Factors
5 Classification and Diagnostic Frameworks	11 Management and Treatment Approaches, NASC, and Support for Patients and Whānau/Carers
6 A Simple Diagnostic Flow	12 Severe-Very Severe ME Care

Clinicians are also encourage to explore:

• Clinical Education (CME/CPD)
• Resources
• Clinical Events

And to refer patients and whānau to: Support Groups & Service Providers

Myalgic Encephalomyelitis (ME) and Long COVID with ME-like Features

Myalgic Encephalomyelitis (ME) and Long COVID with ME-like features are serious, multi‑system conditions characterised by impaired energy production, autonomic dysfunction, immune dysregulation, and abnormal physiological responses to exertion. They are not psychological disorders, and they require careful clinical recognition, early management, and avoidance of interventions that may cause harm — particularly those that increase exertion beyond the patient’s physiological limits.

Clinicians play a vital role in:

• recognising hallmark features such as Post-Exertional Malaise (PEM) known as Post-Exertional Symptom Exacerbation (PESE) in Long COVID
• applying evidence‑based diagnostic criteria
• ruling out alternative causes and identifying common co‑morbidities
• supporting patients with safe, symptom‑contingent management
• preventing deterioration through early pacing and avoidance of graded exercise
• coordinating care across disciplines and advocating for appropriate supports

Biomedical Mechanisms

Pathophysiological Pathways: ME and Long COVID with ME-like features involve multi‑system physiological abnormalities. These domains are well‑supported by international research and help clinicians understand why exertion intolerance, cognitive dysfunction, autonomic symptoms, and multi‑organ complaints occur.

Post-Viral Onset Patterns

ME and Long COVID with ME‑like features frequently follow:

• acute viral infections
• repeated viral exposures
• immune challenges
• other physiological stressors (surgery, trauma, allergic reactions, toxic exposure, other environmental triggers)

Long COVID has provided a large, contemporary cohort demonstrating classic ME onset patterns, including exertion intolerance, autonomic dysfunction, and persistent post‑viral symptoms.

Symptom Clusters

Clinicians increasingly recognise ME and LC with ME‑like features through core symptom clusters:

• PEM/PESE
• fatigue and energy impairment
• cognitive dysfunction
• sleep disturbance
• pain
• autonomic symptoms
• immune / flu‑like symptoms

These clusters help differentiate ME from conditions such as depression, FND, thyroid disorders, anaemia, and other differential diagnoses.

Classification and Diagnostic Frameworks

ME and LC with ME‑like features require accurate, evidence‑based diagnostic frameworks that reflect current biomedical understanding. Below is a concise, clinician‑friendly overview of the major classification systems, their strengths and limitations, and the recommended diagnostic approach for primary care.

World Health Organisation (WHO) Classification

Diagnostics

2015: Institute of Medicine (IoM)

The Institute of Medicine (IoM) now named the National Academy of Medicine (NAM) 2015 criteria are now the preferred diagnostic framework for primary care because they are:

• simple
• clinically practical
• biomedically accurate
• aligned with NICE 2021
• validated across ME and LC with ME‑like features

Diagnosis requires all three core symptoms, plus one of two additional symptoms:

Core symptoms (all required):

1. Substantial reduction or impairment in pre-illness activity (lasting >6 months in adults, <3 months in youth/adolescents) coupled with Profound Fatigue of New Onset that cannot be explained by other causes.
2. Post‑exertional malaise (PEM)
3. Unrefreshing sleep

Plus one of:

• Cognitive impairment, or
• Orthostatic intolerance

This framework captures the symptom clusters seen in ME and is feasible within standard GP appointment timeframes. Most patients experience both the two additional criteria (cognitive impairment AND orthostatic intolerance) but only one is required for diagnosis.

Long COVID Diagnostic Criteria

Long COVID is diagnosed when symptoms persist 12 weeks or more after a confirmed or suspected SARS‑CoV‑2 (COVID-19) infection and cannot be explained by an alternative diagnosis. The condition is heterogeneous, but a large subgroup develops LC with ME‑like features, characterised by exertion intolerance, autonomic dysfunction, cognitive impairment, and multi‑system symptoms.

Long COVID with ME-like Features

A clinically important subgroup presents with:

• PEM/PESE
• activity intolerance
• autonomic dysfunction (including POTS/OI)
• cognitive impairment
• sleep disturbance
• pain
• immune / flu‑like symptoms

These patients often meet IOM/NAM (2015) criteria for ME within 6–12 months of onset.

A Simple Diagnostic Flow for Busy Clinicians

A streamlined diagnostic approach suitable for general practice:

Visit ANZMES Best Practice Guidelines.

Historical Context: How ME was Misclassified as Psychological

ME has a long and well‑documented history as a post‑infectious neurological condition, recognised across multiple outbreaks and formally classified by the World Health Organization in 1969. However, a single unsubstantiated psychological theory published in 1970 as an “opinion piece” derailed decades of research, funding, and clinical care. Understanding this history helps clinicians recognise why outdated models persist and why modern biomedical frameworks are essential.

Early Recognition of Post-Viral, Neurological Illness

Modern Biomedical Evidence

Thanks to decades of perseverance from patients, clinicians, and researchers, ME is now recognised as a multi‑system biomedical condition involving:

• impaired energy metabolism
• mitochondrial dysfunction
• autonomic nervous system impairment
• immune dysregulation
• neuroinflammation
• post‑viral onset patterns
• abnormal physiological responses to exertion (PEM/PESE)

These findings are consistent across ME and LC with ME‑like features, and they align with international consensus frameworks such as NICE 2021, IOM/NAM 2015, CCC, and ICC.

The modern evidence base clearly demonstrates that ME is not a psychological disorder, and psychological interventions cannot treat or cure the underlying pathophysiology.

Why this History Matters for Clinicians and their Patients

Understanding this history helps clinicians:

• recognise why outdated models persist in some settings
• avoid harmful interventions such as GET
• apply modern diagnostic criteria grounded in biomedical evidence
• provide safe, compassionate, and effective care
• support patients who may have experienced stigma or dismissal
• engage confidently with contemporary research and guidelines

Clinicians are encouraged to review ANZMES’ guide on evaluating evidence quality: Discerning Robust vs Flawed Science

Differential Diagnoses: Rule-Outs and Multi-morbidities

ME and LC with ME‑like features require careful clinical assessment to distinguish them from other conditions that present with fatigue, cognitive symptoms, sleep disturbance, pain, or autonomic complaints. Accurate diagnosis depends on recognising PEM/PESE, applying IOM/NAM (2015) criteria, and ruling out alternative causes.

Essential Rule-Outs for Clinicians

These conditions may mimic aspects of ME or LC with ME‑like features. Ruling them out ensures diagnostic accuracy and prevents misclassification.

Common Multi-morbidities

Many patients with ME or LC with ME‑like features experience overlapping conditions. Recognising these helps clinicians provide comprehensive care.

• Dysautonomia Orthostatic intolerance/POTS, tachycardia, dizziness, palpitations.
• Mast Cell Activation Syndrome (MCAS) Flushing, hives, GI symptoms, sensitivities.
• Migraine Common in ME and LC cohorts; often worsened by sensory load.
• IBS / GI Dysmotility Gastroparesis, constipation, diarrhoea, abdominal pain.
• Fibromyalgia Widespread pain, sensory amplification, sleep disturbance.
• Sleep Disorders Insomnia, hypersomnia, circadian rhythm disruption.
• Secondary Mood Impacts Emotional distress arising from chronic illness, not causative.

The Research “Pentad”

Research cohorts frequently identify a Pentad of conditions commonly co‑occurring with ME:

• Fibromyalgia (FM)
• POTS / Orthostatic Intolerance (OI)
• Migraine disorders
• IBS / GI dysmotility
• MCAS or hEDS, depending on cohort characteristics

These reflect shared autonomic, connective tissue, immune, and sensory dysregulation.

The Clinical “Septad”

The “Septad” (Kaufman and Ruhoy) describes a broader constellation of overlapping conditions frequently seen in ME and LC with ME‑like features, and is increasingly recognised in clinical practice in New Zealand:

• Dysautonomia (OI, POTS, NMH, IST)
• Mast Cell Activation Syndrome (MCAS)
• Hypermobile Ehlers‑Danlos Syndromes (hEDS) / EDS
• Gastrointestinal issues (IBS, gastroparesis, dysmotility)
• Autoimmune conditions
• Chronic viral reactivation
• Neurologic structural issues (small fibre neuropathy, craniocervical instability)

These conditions share underlying patterns of autonomic dysfunction, immune dysregulation, connective tissue fragility, and sensory hypersensitivity.

Emerging research is also linking ME and these complex chronic conditions with compression syndromes (e.g. May Thurner, Nutcracker, MALS, etc.), endometriosis, and neurodivergence.

Why This Matters

Understanding differential diagnoses, multi‑morbidities, and symptom clusters helps clinicians:

• avoid misdiagnosis
• recognise ME early
• differentiate ME from psychiatric or functional conditions
• identify treatable co‑morbidities
• tailor management plans
• prevent deterioration through safe, symptom‑contingent care

Causes and Aetiology

ME and LC with ME‑like features are understood as post‑infectious, multi‑system conditions arising from a complex interaction of biological vulnerability and physiological stressors. While the precise aetiology remains under investigation, contemporary evidence provides a clear picture of the major contributing pathways.

Unknown Aetiology but NOT Unknown Mechanisms

The exact initiating mechanism is not fully defined, but ME is not idiopathic in the traditional sense. Across decades of research, consistent patterns show:

• post‑viral onset
• immune dysregulation
• autonomic nervous system impairment
• mitochondrial dysfunction
• neuroinflammation
• abnormal physiological responses to exertion (PEM/PESE)

These findings demonstrate a biomedical, not psychological, origin.

Predominately Post-Viral

The majority (~80%) of ME cases follow an acute viral illness. Common triggers include:

• Epstein–Barr virus (EBV)
• Influenza
• Enteroviruses
• SARS‑CoV‑2
• Other respiratory or systemic viral infections

Long COVID has provided a large, contemporary cohort demonstrating classic ME onset patterns, including exertion intolerance, autonomic dysfunction, and persistent post‑viral symptoms.

Other Recognised Triggers

Although viral infections are the most common, other physiological stressors can precipitate ME or LC with ME‑like features:

• bacterial infections
• immune challenges
• surgery or anaesthesia
• trauma
• environmental stressors
• toxic chemical exposures

These triggers appear to interact with underlying biological vulnerability, tipping multiple systems into dysregulation.

Genetic Predisposition and Risk Factors

Emerging evidence suggests that some individuals may have genetic or biological predispositions that increase susceptibility to post‑viral dysregulation. Risk factors include:

• family history of autoimmune conditions
• childhood viral illness (e.g., glandular fever)
• repeated viral exposures
• pre‑existing autonomic fragility
• connective tissue disorders (e.g., hEDS)
• an additional environmental stressor (trigger)

These factors do not cause ME on their own but may influence how the body responds to infection or physiological stress.

Management and Treatment Approaches

Management of ME and LC with ME‑like features centres on symptom‑contingent pacing, prevention of deterioration, and targeted support for autonomic, sleep, pain, and cognitive symptoms. There is no curative treatment, and interventions must avoid triggering PEM/PESE, the hallmark physiological abnormality.

This section provides clinicians with safe, evidence‑aligned strategies for supporting patients across all severity levels.

Although ME and LC with ME‑like features are primarily managed in general practice, safe and effective care is multidisciplinary. No single clinician can meet the full spectrum of patient needs. Management is strongest when GPs work collaboratively with:

• Health Improvement Practitioners (HIPs)
• Nurse Practitioners / Practice Nurses
• Occupational Therapists (OTs)
• Physiotherapists (for pacing, autonomic support — not graded exercise)
• Counsellors / Psychologists (for adjustment, stress, secondary mood impacts)
• Breathing specialists (particularly for LC‑related dyspnoea)
• Pain management practitioners (e.g., massage therapists, acupuncture, CBT‑based pain coping)
• Allied and integrative health providers who understand PEM/PESE and avoid exertion‑based approaches

This collaborative model supports stabilisation, reduces deterioration, and helps patients manage the complex, multi‑system nature of ME and LC with ME‑like features.

Core Principles

Symptom‑Contingent Pacing (Not Quota‑Based Activity)

Pacing is the cornerstone of management. It involves:

• identifying individual energy limits
• preventing PEM/PESE
• balancing activity with rest
• reducing sensory load
• shaping activity gradually only when stable

Patients should be encouraged to stop before symptoms escalate, not push through fatigue.

Activity Diary and Load Mapping

Clinicians can support patients to:

• track physical, cognitive, and sensory activities
• identify PEM triggers
• map daily energy patterns
• adjust routines to reduce crashes

This helps patients visualise their “energy envelope” and stabilise symptoms.

Chunking and Energy Envelope Management

Patients benefit from:

• breaking tasks into smaller components
• spreading activity across the day
• alternating high‑load and low‑load tasks
• incorporating pre‑emptive rest

This reduces physiological stress and supports stability.

Heart-Rate Monitoring

Heart rate monitoring can help patients avoid exceeding their anaerobic threshold, which often triggers PEM/PESE. Clinicians may discuss:

• using wearable devices
• identifying heart rate spikes associated with symptoms
• adjusting activity to remain within safe limits

This is not an exercise programme; it is a protective strategy to prevent deterioration.

Activity Shaping

Once patients achieve stability (fewer crashes, predictable energy patterns), clinicians may support gentle shaping:

• only within the patient’s safe zone
• only when PEM/PESE is controlled
• only with patient‑led adjustments
• never using graded exercise therapy (GET)

Shaping is not graded exercise. It is a cautious, symptom‑contingent approach.

Pharmacological Support

There is no curative medication, but targeted pharmacological support can improve quality of life. Clinicians may consider category‑level options for:

• Pain: Neuropathic pain agents, migraine management, musculoskeletal support.
• Sleep: Sleep hygiene, circadian rhythm support, short‑term pharmacological aids when appropriate.
• Autonomic Dysfunction / POTS: Volume expansion strategies, autonomic stabilisation, symptom‑targeted medications, beta blockers.
• MCAS: Antihistamines, mast‑cell stabilisers, GI symptom management.
• GI Dysmotility: Prokinetics, antiemetics, IBS management.
• Mood Impacts: Support for secondary anxiety or depression related to chronic illness.

Clinicians should tailor approaches to individual symptom profiles and co‑morbidities.

Needs Assessment and Service Coordination (NASC)

Patients with ME or LC with ME‑like features often experience significant functional impairment, particularly in ADLs and IADLs. When impairment becomes severe, clinicians may need to consider NASC referral to support safe living conditions, reduce carer strain, and prevent deterioration. The following guidance helps clinicians document functional limitations accurately and navigate the NASC process, which remains highly variable across regions.

NASC is a government‑funded service that assesses a person’s needs to determine eligibility for publicly funded home‑based support. It is accessed through Long Term Supports – Chronic Health Conditions (LTS‑CHC).

NASC can provide access to:

• Home Management (cleaning, laundry, meal support)
• Personal Care (showering, dressing, toileting)
• Carer Support (respite allocations)

These supports are essential for preserving a patient’s Energy Envelope, reducing carer burden, and preventing deterioration.

Important Clinical Note: Eligibility is extremely limited

In Aotearoa, NASC criteria vary by region, but are generally restricted to:

• people requiring continuous support (often described as 24/7 care), for whom up to 21 hours per week may be granted
• people who are predominantly bedbound
• people with severe dysautonomia, very low functional capacity, or high risk of harm without assistance

Access for ME/CFS patients is inconsistent across the motu. Some regions recognise the needs of those who are housebound or severely limited; others do not. This creates a postcode lottery, where two patients with identical impairment may receive very different levels of support depending on where they live.

Accurate documentation of functional impairment is critical. When referring to NASC, include:

• frequency and severity of PEM crashes
• inability to perform ADLs without deterioration
• orthostatic intolerance and safety risks
• cognitive impairment affecting medication management
• carer strain and whānau impact
• risk of hospitalisation if support is not provided

Clear clinical language can make the difference between a declined application and essential support.

Clinical Reference: ADLs vs IADLS (A quick guide for documenting functional impairment in ME or LC with ME-like features) Activities of Daily Living (ADLs) In ME, ADL impairment is often intermittent but severe — clinicians should document the frequency, predictability, and post‑exertional consequences of ADL attempts. These are the essential, basic tasks required for personal care and physical safety. Impairment in ADLs is often required for NASC eligibility. ADLs include: – Showering or bathing – Dressing and undressing – Toileting – Feeding oneself – Basic grooming – Transferring (e.g., getting in/out of bed or a chair) – Mobility within the home In ME: Patients may be unable to complete ADLs without triggering post‑exertional malaise (PEM), orthostatic symptoms, or collapse. Even “simple” tasks can exceed their physiological capacity. Instrumental Activities of Daily Living (IADLs) Loss of IADLs often precedes ADL impairment and is an early indicator of functional decline.  These are more complex tasks required for independent living. Some regions consider IADL impairment for Home Management support; others do not. IADLs include: – Cleaning – Laundry – Meal preparation – Shopping – Managing medications – Managing finances – Transport and community access In ME: IADLs are often the first tasks patients lose due to limited energy, cognitive impairment, and orthostatic intolerance. Why this matters for clinicians Clear documentation of ADL and IADL impairment helps NASC understand the real‑world functional impact of ME/CFS. Include: – frequency and severity of PEM – inability to complete ADLs without deterioration – safety risks (falls, syncope, cognitive lapses) – carer strain and whānau impact – the patient’s baseline, not their “best day” This information can be the difference between declined support and essential care.

NASC support does not replace clinical management; it complements pacing, autonomic stabilisation, and multidisciplinary care by reducing the daily load that triggers PEM/PESE. 

Counselling and Therapy:

• Specialised psychological support focused on adjusting to Long Term Conditions, grief for one’s former life, and managing the trauma of medical skepticism.
• Supports mental health without the goal of “curing” the physical disease through “positive thinking.”

Support for Patients and Whānau/Carers

People living with ME or LC with ME‑like features often require support that extends beyond clinical care. Social connection, practical assistance, and informed whānau involvement can significantly improve stability, reduce isolation, and help patients manage the day‑to‑day realities of a fluctuating, disabling condition.

Clinicians play an important role in connecting patients and families with appropriate community‑based supports.
Support Groups & Community Networks
Patients and whānau benefit from:

• peer support
• shared lived experience
• practical strategies for pacing and daily management
• emotional validation
• connection with others who understand the condition

Clinicians can refer patients to organisations and individuals throughout the motu who provide safe, evidence‑aligned support:

Support Groups & Service Providers

These groups offer social connection, carer support, and community resources that complement clinical care.

Whānau & Carer Support

Whānau often take on significant caregiving roles, especially for patients with moderate, severe, or very severe ME. Clinicians can help by:

• acknowledging the burden of care
• providing clear guidance on pacing and symptom‑contingent support
• helping families understand PEM/PESE
• encouraging low‑stimulus environments for severe ME
• directing carers to community resources and respite options where available

Support for carers improves patient outcomes and reduces burnout.

Practical Resources

Clinicians may also direct patients and whānau to:

• management tools (activity diaries, pacing guides)
• autonomic support strategies
• nutrition and hydration guidance
• sleep and sensory‑load management resources
• education modules for both clinicians and patients

These resources help patients build sustainable routines and reduce the frequency and severity of crashes.

When to Seek Additional Help

Patients and whānau should be encouraged to seek further support when:

• symptoms escalate or become unpredictable
• PEM/PESE becomes more frequent
• autonomic symptoms worsen
• nutritional intake declines
• care demands exceed what is safe at home
• the patient shows signs of severe or very severe ME

Clinicians can refer to ANZMES’ severe ME guidance for hospital considerations and stabilisation strategies below.

Severe-Very Severe ME Care

Severe and very severe ME represent the extreme end of the illness spectrum, where patients experience profound physiological depletion and multi‑system dysfunction. This is not psychological. These patients often cannot:

• speak
• swallow
• tolerate light or sound
• sit upright
• move without triggering deterioration
• manage basic activities of daily living

Hypersensitivity to sensory input is common and reflects neurological and autonomic dysregulation, not anxiety or avoidance.
Patients with severe or very severe ME require specialised, low‑stimulus care:

• minimise sensory input (light, sound, touch)
• avoid unnecessary movement or repositioning
• provide quiet, predictable routines
• support feeding, hydration, toileting
• consider home‑based care when possible
• avoid hospital environments unless essential

Severe ME patients may be unable to speak, tolerate light, or sit upright. Care must be adapted accordingly.

Hospital Considerations

Hospitalisation for ME is not about rehabilitation or improvement. It is almost always required because the patient has:

• experienced a crash
• become unsafe at home
• developed severe dehydration
• requires IV hydration or electrolytes
• needs nutritional support to prevent under‑nutrition or malnutrition
• requires pain management
• needs monitoring for complications (e.g., orthostatic instability, GI failure)

The clinical goal is stabilisation, not exertion‑based recovery. Hospital environments can worsen symptoms due to sensory overload, frequent interruptions, and movement demands. Care must be adapted to the patient’s tolerance. Therefore hospitalisation can be dangerous for ME patients due to sensory overload, exertion demands, and unfamiliar routines. Clinicians should:

• provide a low‑stimulus environment
• reduce noise, light, and interruptions
• avoid physiotherapy‑led exertion programmes
• ensure staff understand PEM/PESE
• allow flexible positioning
• consider IV fluids for orthostatic intolerance or poor oral intake
• avoid unnecessary investigations that require exertion

Refer to ANZMES’ dedicated severe-very severe ME guidance.