FAILURES OF THE UK ME ASSOCIATION TOWARD THE ROYAL FREE/RAMSAY - "MYALGIC ENCEPHALOMYELITIS" PATIENT POPULATION
FAILURES OF THE UK ME ASSOCIATION TOWARD THE ROYAL FREE/RAMSAY - "MYALGIC ENCEPHALOMYELITIS" PATIENT POPULATION
PREMISE AND SCOPE
For this critique, "M.E." means:
ROYAL FREE DISEASE /
MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS)
classified under the proposed umbrella:
ATYPICAL POLIOMYELITIS.
It does NOT mean:
CFS;
ME/CFS;
SEID;
Unexplained Generalised Fatigue;
...or a disease defined solely by Post-Exertional Malaise.
CORE DISEASE DISTINCTION
Royal Free Disease / Myalgic Encephalomyelitis must not be conflated with CFS, ME/CFS or SEID.
Under this framework:
ROYAL FREE DISEASE / M.E.
=
A SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE
...with an infectious/enteroviral disease model and neurological involvement.
By contrast:
CFS
=
A LATER SYMPTOM-DEFINED SYNDROME.
ME/CFS
=
A COMPOUND UMBRELLA TERM USED ACROSS LATER SYMPTOM-DEFINED POPULATIONS.
SEID
=
A LATER SYMPTOM-DEFINED DIAGNOSTIC CONSTRUCT.
These later constructs are not demonstrated synonyms for Royal Free Disease.
They are not demonstrated synonyms for Ramsay-defined Myalgic Encephalomyelitis.
They do not require the same:
Sudden neurological onset;
Infectious aetiology;
Enteroviral infection;
Encephalitis;
Encephalomyelitis;
Objective acute CNS disease;
Neurological phenotype;
Motor-fatigability pattern;
or clinical course.
The essential nosological distinction is therefore:
ROYAL FREE DISEASE / M.E.
=
A SPECIFIC "SUDDEN-ONSET" NEUROLOGICAL DISEASE ENTITY.
CFS / ME/CFS / SEID
=
LATER SYMPTOM-BASED DIAGNOSTIC CONSTRUCTS.
A later symptom definition cannot retrospectively establish that it is the same disease as the earlier Royal Free/Ramsay neurological entity.
Putting "M.E." beside "CFS" does not prove biological equivalence.
Calling a SEID/IOM-style population "ME/CFS" does not turn it into Royal Free Disease.
Therefore:
M.E. ≠ (is NOT) CFS.
M.E. ≠ (is NOT) ME/CFS.
M.E. ≠ (is NOT) SEID.
THESE TERMS SHOULD NOT BE USED INTERCHANGEABLY.
The proposed clinical classification is:
ATYPICAL POLIOMYELITIS
01. MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS) / ASEPTIC MENINGITIS
(ENTEROVIRAL MENINGOENCEPHALOMYELITIS)
02. ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME
These terms are intended to make the neurological and infectious-disease framework immediately clear to the treating doctor.
The defining clinical framework is not:
UNEXPLAINED GENERALISED FATIGUE
+
POST-EXERTIONAL MALAISE.
Instead:
SUDDEN INFECTIOUS/NEUROLOGICAL ONSET
↓
ENTEROVIRAL ENCEPHALOMYELITIS
↓
CENTRAL NERVOUS SYSTEM DYSFUNCTION
+
AUTONOMIC DYSFUNCTION
↓
CENTRAL FATIGUE
↓
ABNORMAL MUSCLE FATIGABILITY
↓
POST-EXERTIONAL MOTOR WEAKNESS
↓
DELAYED RESTORATION OF MUSCLE POWER.
Generalised fatigue does not have to be the prominent feature when the patient suddenly becomes ill.
The acute presentation may instead be dominated by neurological, autonomic, motor, bulbar, sensory or gastrointestinal dysfunction.
Therefore:
CENTRAL FATIGUE ≠ (is NOT) UNEXPLAINED GENERALISED FATIGUE.
MUSCLE FATIGABILITY ≠ (is NOT) SUBJECTIVE TIREDNESS or GENERALISED FATIGUE.
MOTOR WEAKNESS ≠ (is NOT) MALAISE.
DELAYED RESTORATION OF MUSCLE POWER ≠ (is NOT) PEM.
The central criticism of the ME Association is therefore not simply that it "hasn't done enough."
It is that an organisation historically associated with representing this specific disease population progressively failed to preserve:
The identity of the disease;
The distinction between a specific neurological disease and later symptom-defined constructs;
The original Royal Free/Ramsay patient cohort;
Its sudden-onset neurological presentation;
Its infectious/enteroviral disease framework;
Its CNS and autonomic manifestations;
Its defining motor-fatigability framework;
Its potential neurological severity;
Its appropriate diagnostic pathway;
Its disease-specific research;
Its specialist services;
Its treatment-development priorities;
Its patient representation;
Its research-funding integrity;
And its charitable accountability.
I. LOSS OF THE DISEASE THE ORGANISATION WAS SUPPOSED TO REPRESENT
1. FAILURE TO PRESERVE M.E. AS A DISTINCT NEUROLOGICAL DISEASE
The Association's first responsibility should have been protecting the identity of Royal Free/Ramsay M.E.
Instead, M.E. became progressively entangled with CFS and subsequently broader diagnostic constructs.
Under this framework, this was not merely terminology.
It represented a potential substitution of:
A SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE
with
LATER SYMPTOM-DEFINED DIAGNOSTIC POPULATIONS.
Changing the diagnostic construct potentially changes:
Who is diagnosed;
Which patients enter research;
Epidemiology;
Clinical trials;
Medical services;
Treatment recommendations;
Funding priorities;
Public understanding.
2. FAILURE TO DEFEND "MYALGIC ENCEPHALOMYELITIS"
The ME Association historically supported use of "Myalgic Encephalopathy," including arguments concerning greater acceptability of that terminology to doctors.
Under this critique, this was backwards.
If doctors disputed encephalomyelitis, the appropriate response should have been:
IDENTIFY GENUINE M.E.
↓
INVESTIGATE CNS DISEASE
↓
ESTABLISH OR REFUTE ENCEPHALOMYELITIS
↓
FOLLOW THE EVIDENCE
↓
DEFEND THE DIAGNOSIS IF SUPPORTED.
Medical disbelief should not determine disease nomenclature.
3. FAILURE TO INVESTIGATE ENCEPHALOMYELITIS ADEQUATELY
If encephalomyelitis was disputed, that created a research question.
The Association should have promoted systematic investigation of appropriately selected Royal Free/Ramsay patients using, where appropriate:
Detailed neurological examination;
Acute brain MRI;
Spinal MRI;
Segami Oasis Neurogam SPECT;
CSF investigation;
Virology;
Electrophysiology;
Longitudinal neurological investigation;
Neuropathology where available.
4. FAILURE TO PROTECT THE ORIGINAL COHORT FROM POPULATION SUBSTITUTION
Failure to demonstrate encephalomyelitis across a broader chronic population cannot establish its absence from Royal Free/Ramsay M.E. unless the populations have first been demonstrated to represent the same disease.
Otherwise:
BROADEN THE POPULATION
↓
FAIL TO FIND THE ORIGINAL PATHOLOGY THROUGHOUT THAT POPULATION
↓
USE THAT RESULT TO QUESTION THE ORIGINAL DISEASE.
That creates a fundamental cohort-selection problem.
It also creates the possibility that research performed in symptom-defined CFS, ME/CFS or SEID populations is being used to answer questions about a separately defined sudden-onset neurological disease.
5. FAILURE TO PROTECT M.E. FROM CFS
Under this framework:
M.E. ≠ (is NOT) CFS.
Royal Free/Ramsay M.E. is being treated here as a specific sudden-onset neurological disease.
CFS is a later syndrome construct based upon symptoms and chronicity.
The boundary should therefore have remained:
M.E. research → M.E. patients.
CFS research → CFS patients.
Evidence from one population should not automatically have been attributed to the other.
6. ACCEPTANCE OF "ME/CFS"
Combining two diagnostic labels does not establish biological equivalence.
"ME/CFS" cannot itself demonstrate that the underlying populations have the same:
Aetiology;
Pathology;
Neurological phenotype;
Onset;
Natural history;
Treatment response.
The letters "M.E." appearing beside "CFS" cannot convert a symptom-defined CFS population into Royal Free/Ramsay M.E.
Under this framework, use of "ME/CFS" as though it were synonymous with Royal Free Disease represents a fundamental nosological error.
7. FAILURE TO KEEP 'SEID' SEPARATE FROM M.E.
Under this framework:
SEID ≠ (is NOT) M.E.
SEID is a later symptom-defined diagnostic construct.
A symptom-defined algorithm cannot itself demonstrate encephalomyelitis or establish that somebody belongs to the Royal Free/Ramsay disease population.
SEID does not require the specific sudden-onset neurological disease being described here.
II. TERMINOLOGY, NOSOLOGY AND CORRECT CLINICAL CLASSIFICATION
8. FAILURE TO PREVENT "ME/CFS" FROM BEING USED AS A SYNONYM FOR ROYAL FREE DISEASE
Under this framework, "ME/CFS" must not be interpreted as meaning the same disease as:
ROYAL FREE DISEASE
or
MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS).
The compound term represents a later diagnostic construction.
It must not retrospectively redefine the Royal Free disease population.
It must not be assumed to represent Ramsay-defined M.E.
It must not be used to replace the diagnosis of a specific sudden-onset neurological disease.
9. FAILURE TO DISTINGUISH A SPECIFIC DISEASE ENTITY FROM SYMPTOM-DEFINED CONSTRUCTS
The fundamental distinction should have been made explicit to patients, doctors, researchers and policy-makers:
ROYAL FREE DISEASE / M.E.
=
SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE.
CFS
=
SYMPTOM-DEFINED SYNDROME.
ME/CFS
=
COMPOUND UMBRELLA TERMINOLOGY.
SEID
=
SYMPTOM-DEFINED DIAGNOSTIC CONSTRUCT.
These are not interchangeable entities.
Symptom criteria can group together patients with different underlying diseases.
They cannot establish that all people satisfying those criteria have the same pathology as a separately defined neurological disease.
10. FAILURE TO MAKE CLEAR THAT "SEID" IS NOT M.E.
Under this framework, SEID is not another name for "Myalgic Encephalomyelitis".
It does not require:
Sudden neurological onset;
Encephalitis;
Encephalomyelitis;
Enteroviral infection;
Acute CNS disease;
Viral detection at onset;
Enteroviral meningoencephalomyelitis;
Poliomyelitis-like neurological disease;
Ramsay's motor-fatigability phenotype.
Therefore:
SEID ≠ (is NOT) ROYAL FREE DISEASE.
SEID ≠ (is NOT) MYALGIC ENCEPHALOMYELITIS.
SEID ≠ (is NOT) ENTEROVIRAL ENCEPHALOMYELITIS.
11. FAILURE TO DISTINGUISH NICE NG206 FROM ACTUAL ROYAL FREE/RAMSAY M.E.
Under this critique, NICE's 2021 guideline does not operationally define the sudden-onset disease being described here.
It does not require:
Sudden neurological onset;
Encephalomyelitis;
Documented enteroviral infection;
Objective acute CNS disease;
Acute viral detection;
Enteroviral meningoencephalomyelitis;
Enteroviral poliomyelitis-like disease;
The Ramsay-defined motor-fatigability framework.
A patient satisfying NG206 has satisfied NG206.
That does not, by itself, establish Royal Free/Ramsay M.E.
Under this framework, NICE NG206 represents a chronic symptom-defined diagnostic pathway rather than a diagnostic pathway for the specific sudden-onset neurological disease being described here.
12. FAILURE TO PROTECT PATIENTS FROM MISDIAGNOSIS THROUGH BROAD SYMPTOM CRITERIA
If Royal Free/Ramsay M.E. is a specific sudden-onset neurological disease, broad symptom-based definitions can produce two opposite diagnostic problems:
PEOPLE WITHOUT ROYAL FREE/RAMSAY M.E. CAN BE LABELLED AS HAVING "M.E."
while
PEOPLE WITH THE ACTUAL SUDDEN-ONSET NEUROLOGICAL DISEASE CAN BE MISSED BECAUSE THEY DO NOT PRESENT WITH GENERALISED FATIGUE OR PEM AS THE DOMINANT FEATURES.
Under this framework, both represent diagnostic distortion.
13. FAILURE TO USE CLINICALLY MEANINGFUL TERMINOLOGY
Under the proposed framework, the clearer umbrella terminology is:
ATYPICAL POLIOMYELITIS
01.
MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS) /
ASEPTIC MENINGITIS
(ENTEROVIRAL MENINGOENCEPHALOMYELITIS)
02.
ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME
This terminology is intended to alert a clinician immediately that the disease being described is neurological and enteroviral rather than a symptom-defined chronic-fatigue construct.
14. CATEGORY 01 - MYALGIC ENCEPHALOMYELITIS / ENTEROVIRAL MENINGOENCEPHALOMYELITIS
The proposed first category includes:
Encephalitis;
Brainstem encephalitis / rhombencephalitic disease;
Encephalomyelitis;
Aseptic meningitis;
Meningoencephalitis;
Meningoencephalomyelitis;
Cranial-nerve dysfunction;
Bulbar dysfunction;
Motor dysfunction;
Autonomic dysfunction;
Central fatigue;
Abnormal muscle fatigability;
Post-exertional motor weakness;
Delayed restoration of muscle power;
Gastrointestinal autonomic dysfunction;
Gastroparesis;
Paralytic ileus;
Other dysmotility;
Cardiac/autonomic involvement.
15. CATEGORY 02 - ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME
The proposed second category includes a predominantly spinal motor-neuron/anterior-horn/poliomyelitis-like presentation.
Potential manifestations include:
Acute flaccid weakness;
Asymmetric paresis;
Motor-neuron injury;
Anterior-horn involvement;
Muscle wasting;
Fasciculations;
Motor weakness;
Reduced motor function;
Bulbar involvement;
Respiratory involvement where severe;
Long-term poliomyelitis-like disability.
The two categories may overlap where both brain/brainstem and spinal motor systems are affected.
16. FAILURE TO USE TERMINOLOGY THAT ALERTS DOCTORS TO THE CORRECT DISEASE
Compare:
"ME/CFS"
with:
"ATYPICAL POLIOMYELITIS -
ENTEROVIRAL MENINGOENCEPHALOMYELITIS"
or:
"ATYPICAL POLIOMYELITIS -
ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME."
The latter terminology immediately directs attention toward:
Neurology;
Infectious diseases;
Enteroviruses;
Brain and spinal cord disease;
CNS investigation;
Motor dysfunction;
Autonomic dysfunction;
Viral persistence;
Severe neurological disability;
Appropriate acute investigation.
17. FAILURE TO PREVENT TERMINOLOGY FROM DOWNGRADING MEDICAL URGENCY
A label centred on fatigue or PEM can obscure the seriousness of sudden CNS disease.
Terminology can influence whether a patient is directed toward:
AN EMERGENCY NEUROLOGICAL / INFECTIOUS-DISEASE PATHWAY
or
A CHRONIC FATIGUE-MANAGEMENT PATHWAY.
That distinction can be clinically consequential.
III. FAILURE TO PRESERVE THE DEFINING NEUROLOGICAL FRAMEWORK
18. FAILURE TO DISTINGUISH CENTRAL FATIGUE FROM GENERALISED FATIGUE
Central fatigue is not synonymous with general fatigue or tiredness.
Within this framework, central fatigue concerns impaired CNS ability to initiate or sustain voluntary motor activity.
Therefore:
CENTRAL FATIGUE ≠ (is NOT) UNEXPLAINED GENERALISED FATIGUE.
19. FAILURE TO PRESERVE ABNORMAL MUSCLE FATIGABILITY
The characteristic exertional abnormality should be represented as:
CENTRAL FATIGUE
↓
ABNORMAL MUSCLE FATIGABILITY
↓
POST-EXERTIONAL MOTOR WEAKNESS
↓
DELAYED RESTORATION OF MUSCLE POWER.
This is a neurological/motor framework.
20. FAILURE TO DISTINGUISH MOTOR WEAKNESS FROM "MALAISE"
Motor weakness means reduction in motor power.
Malaise is a broad subjective concept.
Therefore:
POST-EXERTIONAL MOTOR WEAKNESS ≠ (is NOT) POST-EXERTIONAL MALAISE.
21. FAILURE TO PRESERVE DELAYED RESTORATION OF MUSCLE POWER
The prolonged period required for motor function to recover following exertion should remain an important characteristic requiring objective investigation.
22. INAPPROPRIATE REPLACEMENT OF THE MOTOR FRAMEWORK WITH "PEM"
Under this critique, PEM is not the defining feature of Royal Free/Ramsay M.E.
The framework is:
M.E.
=
ENTEROVIRAL ENCEPHALOMYELITIS
with
CNS DYSFUNCTION
+
AUTONOMIC DYSFUNCTION
+
CENTRAL FATIGUE
+
ABNORMAL MUSCLE FATIGABILITY
+
POST-EXERTIONAL MOTOR WEAKNESS
+
DELAYED RESTORATION OF MUSCLE POWER.
NOT:
M.E.
=
PEM.
23. FAILURE TO RECOGNISE THE POST-POLIO-LIKE MOTOR PHENOTYPE
Under this framework, the chronic motor-fatigability phenomenon has conceptual similarities with post-polio fatigue and motor weakness.
Research should investigate:
Central motor drive;
Motor cortex;
Corticospinal pathways;
Brainstem motor systems;
Spinal cord;
Anterior-horn involvement where present;
Peripheral nerves;
Neuromuscular physiology;
Muscle performance;
Post-exertional loss of motor power;
Restoration of muscle power.
24. FAILURE TO RECOGNISE THAT GENERALISED FATIGUE NEED NOT DOMINATE ONSET
A patient can become suddenly ill with substantial neurological and autonomic dysfunction without unexplained generalised fatigue being the principal complaint.
The acute illness may instead be dominated by:
Cognitive/cortical dysfunction;
Brainstem dysfunction;
Motor abnormalities;
Cranial-nerve abnormalities;
Balance/coordination abnormalities;
Sensory disturbance;
Bulbar dysfunction;
Autonomic abnormalities;
Abnormal muscle fatigability;
Motor weakness.
Under this framework, a fatigue-first diagnostic system can therefore select the wrong patient population from the outset.
IV. AUTONOMIC AND GASTROINTESTINAL DYSFUNCTION
25. FAILURE TO REPRESENT AUTONOMIC DYSFUNCTION AS A MAJOR DISEASE DOMAIN
Autonomic dysfunction can affect:
Heart-rate regulation;
Blood-pressure regulation;
Orthostatic tolerance;
Vasomotor regulation;
Temperature regulation;
Sweating;
Gastrointestinal motility;
Bladder function;
Other autonomically regulated systems.
26. FAILURE TO RECOGNISE GASTROINTESTINAL DYSMOTILITY
Neurological/autonomic dysfunction can involve:
Gastroparesis;
Delayed gastric emptying;
Paralytic ileus;
Reduced intestinal motility;
Severe constipation;
Other upper-GI dysmotility;
Other lower-GI dysmotility.
27. FAILURE TO RECOGNISE THE POTENTIAL SERIOUSNESS OF GASTROPARESIS AND ILEUS
Significant dysmotility can impair:
Oral intake;
Hydration;
Nutrition;
Medication absorption;
Bowel function;
Maintenance of body weight.
Severe or acute ileus can constitute a serious medical problem requiring prompt investigation.
28. FAILURE TO ADVOCATE FOR GI AND NUTRITIONAL SERVICES
According to clinical need, affected patients may require:
Gastroenterology;
GI motility investigation;
Gastric-emptying studies;
Investigation of gastroparesis;
Management of ileus;
Specialist nutrition;
Dietetic support;
Enteral feeding;
Parenteral nutrition where medically necessary;
Appropriate inpatient management.
V. FAILURE AT THE POINT PATIENTS BECOME ILL
29. FAILURE TO PRESERVE SUDDEN NEUROLOGICAL ONSET
Under this framework, M.E. begins with acute/sudden neurological disease.
It does not first become M.E. because symptoms have persisted for months.
This distinction separates the disease being described here from later chronic symptom-defined entities.
30. FAILURE TO SECURE AN ACUTE NHS PATHWAY
Depending upon presentation:
EMERGENCY MEDICINE
↓
NEUROLOGY
↓
INFECTIOUS DISEASES
↓
VIROLOGY
↓
CSF INVESTIGATION WHERE INDICATED
↓
BRAIN/SPINAL IMAGING
↓
AUTONOMIC/CARDIAC/RESPIRATORY/GASTROINTESTINAL INVESTIGATION
↓
LONGITUDINAL FOLLOW-UP.
31. FAILURE TO ADVOCATE FOR IMMEDIATE ONSET DIAGNOSTICS
The acute phase can provide a critical diagnostic opportunity.
Appropriate investigation can include:
Viral PCR/detection;
Enterovirus identification;
Enterovirus typing/subtyping;
Throat/respiratory sampling;
Stool testing;
Blood investigation;
CSF virology;
Lumbar puncture where indicated;
Brain MRI;
Spinal MRI;
Neurological examination;
Cardiac investigation;
Autonomic investigation.
32. FAILURE TO CAPTURE THE INITIATING VIRUS
Waiting until chronic illness has developed can make reconstruction of the initiating infection substantially harder.
33. FAILURE TO DOCUMENT CNS DISEASE WHILE IT IS OCCURRING
Failure to perform appropriate investigation during acute CNS disease can result in diagnostic evidence being lost.
A later failure to demonstrate the original process cannot reliably establish that it never occurred.
34. FAILURE TO CREATE PROSPECTIVE ACUTE-ONSET COHORTS
The research pathway should have been:
DOCUMENTED ACUTE ENTEROVIRUS
↓
SUDDEN CNS DISEASE
↓
OBJECTIVE NEUROLOGICAL/AUTONOMIC INVESTIGATION
↓
LONGITUDINAL FOLLOW-UP
↓
VIRAL CLEARANCE OR PERSISTENCE
↓
NEUROLOGICAL, AUTONOMIC AND MOTOR OUTCOME.
VI. FAILURE OF THE ENTEROVIRUS PROGRAMME
35. FAILURE TO PRESERVE THE INFECTIOUS-DISEASE ORIGINS OF ROYAL FREE DISEASE
Royal Free was historically investigated as an outbreak.
That should have kept infectious-disease investigation and outbreak surveillance central.
36. FAILURE TO MAKE ENTEROVIRUS RESEARCH CENTRAL
The major questions should have included:
Which enterovirus?
Which subtype?
Which cells?
Which tissues?
Which CNS structures?
What determines clearance?
What permits persistence?
What neurological pathology follows?
What autonomic pathology follows?
What muscular pathology follows?
What cardiac pathology follows?
How can persistent infection be eradicated?
37. FAILURE TO RESOLVE ENTEROVIRUS PERSISTENCE
Contested research should have generated major independent replication programmes involving:
Tightly characterised cohorts;
Appropriate controls;
Independent laboratories;
Blinding;
Modern molecular virology;
Tissue investigation;
Longitudinal sampling.
38. FAILURE TO CONNECT ACUTE INFECTION WITH CHRONIC PERSISTENCE
The ideal chain is:
VIRUS X AT ONSET
↓
ACUTE CNS DISEASE
↓
FAILURE TO CLEAR VIRUS X
↓
PERSISTENT INFECTION / RESERVOIR
↓
CONTINUING PATHOLOGY
↓
PATHOGEN-DIRECTED TREATMENT
↓
VIROLOGICAL + CLINICAL RESPONSE.
39. FAILURE TO INVESTIGATE RECOVERY VERSUS PERSISTENCE
Why does one patient recover while another develops persistent neurological disease?
That should have been a central prospective research question.
VII. FAILURE TO PURSUE ANTIVIRAL DEVELOPMENT
40. FAILURE TO ADVOCATE AGGRESSIVELY FOR ANTI-ENTEROVIRUS DRUG DEVELOPMENT
If effective treatments do not exist, developing them should become the objective.
The programme should include:
Antiviral discovery;
Viral targets;
Resistance;
CNS/tissue penetration;
Preclinical testing;
Safety;
Virologically selected trials;
Combination therapy where justified.
41. FAILURE TO MAKE PERSISTENT INFECTION THERAPEUTICALLY CENTRAL
If persistence is biologically plausible, it should be directly investigated rather than marginalised by assumption.
42. CREATION OF AN ANTIVIRAL EVIDENCE VACUUM
DON'T DIAGNOSE AT ONSET
↓
DON'T IDENTIFY ENTEROVIRUS
↓
DON'T CREATE PATHOGEN-SPECIFIC COHORTS
↓
DON'T MONITOR CLEARANCE
↓
DON'T ESTABLISH RESERVOIRS
↓
SAY PERSISTENCE ISN'T ESTABLISHED
↓
DON'T PRIORITISE ANTIVIRAL TRIALS
↓
CONTINUE LACKING ANTIVIRAL EVIDENCE.
43. FAILURE TO DISTINGUISH ABSENCE OF EVIDENCE FROM EVIDENCE OF ABSENCE
No licensed antiviral ≠ (does not mean) no infection.
No successful trial ≠ (does not mean) antivirals cannot work.
Negative findings in another population ≠ (does not mean) negative findings in Ramsay M.E.
No virus detected years later ≠ (does not mean) no virus during acute disease.
44. FAILURE TO PROTECT PATIENTS WITH DEMONSTRATED PERSISTENT ENTEROVIRUS
Patients with evidence of persistent infection and neurological disease require appropriate infectious-disease and neurological assessment.
VIII. RESEARCH, RAMSAY AND FUNDING
45. FAILURE TO ESTABLISH GENUINELY M.E.-SPECIFIC RESEARCH COHORTS
A study does not become M.E. research because "M.E." appears in its title.
Its participants must represent the disease being claimed.
Under this framework:
CFS RESEARCH ≠ (is NOT) M.E. RESEARCH.
ME/CFS RESEARCH ≠ (is NOT) M.E. RESEARCH.
SEID RESEARCH ≠ (is NOT) M.E. RESEARCH.
unless participants are independently shown to satisfy the actual Royal Free/Ramsay disease definition being claimed.
46. FAILURE TO ESTABLISH A GENUINE M.E.-SPECIFIC BIOBANK
A disease-specific biobank should preserve:
Sudden onset;
Pathogen information;
Neurological presentation;
Autonomic presentation;
Motor dysfunction;
Imaging;
CSF findings;
Cardiac involvement;
GI dysmotility;
Virology;
Longitudinal progression.
47. FAILURE TO PRESERVE THE DEFINING MOTOR PHENOTYPE
Research should explicitly investigate:
CENTRAL FATIGUE
↓
ABNORMAL MUSCLE FATIGABILITY
↓
POST-EXERTIONAL MOTOR WEAKNESS
↓
DELAYED RESTORATION OF MUSCLE POWER.
This should not be replaced by PEM.
48. FAILURE TO ENSURE RAMSAY-LABELLED RESEARCH INVESTIGATES RAMSAY M.E.
Using Ramsay's name does not make every funded population Ramsay M.E.
49. POTENTIAL MISDIRECTION OF M.E./RAMSAY RESEARCH FUNDING
An independent audit should establish:
How much money was raised using M.E./Ramsay branding?
Which studies received it?
Which criteria were used?
How many required Ramsay-defined M.E.?
How much supported CFS, ME/CFS, SEID-style or other populations?
What did donors understand they were funding?
Were funds legally restricted?
A criminal allegation of fraud would require separate proof of dishonesty and the applicable legal elements.
IX. FAILURE OF PATIENT REPRESENTATION
50. FAILURE TO ENSURE RAMSAY-DEFINED PATIENTS ARE REPRESENTED THROUGHOUT THE CHARITY
Meaningful representation should exist within:
Trustee/board governance;
Strategic leadership;
Medical/scientific policy;
Research committees;
Ramsay Research Fund decisions;
Grant assessment;
Nomenclature decisions;
NHS advocacy;
Public communications;
Stakeholder representation.
51. FAILURE TO GIVE PATIENTS POWER OVER THE IDENTITY OF THEIR OWN DISEASE
Patients should have been able to challenge:
Why is Encephalomyelitis becoming Encephalopathy?
Why is M.E. being combined with CFS?
Why are later symptom-based constructs being treated as equivalent to a sudden-onset neurological disease?
Why is PEM replacing the neurological motor framework?
Why isn't sudden neurological onset central?
Why isn't enterovirus identified?
Why aren't antivirals prioritised?
Why are other populations being researched under Ramsay/M.E. identity?
52. FAILURE TO GIVE RAMSAY PATIENTS INFLUENCE OVER FUNDING DECISIONS
Patients should participate directly in determining:
What constitutes M.E. research;
Which grants receive funding;
Which cohort definitions are acceptable;
Whether onset diagnostics are prioritised;
Whether enterovirus receives major funding;
Whether persistence receives major funding;
Whether antiviral development receives major funding.
X. FAILURE TOWARD THE MOST SEVERELY AFFECTED
53. FAILURE TO PROTECT THE MOST SEVERELY INJURED, DISABLED AND ILL
Severe disease can involve profound:
Neurological dysfunction;
Motor impairment;
Autonomic dysfunction;
Sensory abnormalities;
Cognitive dysfunction;
Bulbar dysfunction;
GI dysmotility;
Nutritional compromise;
Systemic complications.
54. FAILURE TO SECURE APPROPRIATE SPECIALIST SERVICES
According to clinical need:
Neurology;
Infectious diseases;
Autonomic medicine;
Cardiology;
Respiratory medicine;
Gastroenterology;
GI motility services;
Nutrition;
Rehabilitation;
Home care;
Disability services;
Hospital care.
55. FAILURE TO PROVIDE SERVICES FOR SEVERE GI/AUTONOMIC DISEASE
Patients with severe gastroparesis, paralytic ileus or major dysmotility may require specialist investigation, nutritional support and inpatient management.
56. FAILURE TO PROTECT PATIENTS BEFORE CRISIS
Services should exist before somebody develops:
Severe malnutrition;
Dehydration;
Dangerous GI dysfunction;
Respiratory compromise;
Severe neurological deterioration;
Profound immobility;
Other medical crises.
XI. FAILURE OF PUBLIC MEDICAL INFORMATION
57. FAILURE TO PROVIDE AN ACCURATE ROYAL FREE/RAMSAY DISEASE DESCRIPTION
Under this framework, public information should explain that Royal Free Disease / M.E. is being described as a specific sudden-onset neurological disease rather than a broad symptom-defined chronic syndrome.
Information should explain:
Sudden onset;
Enteroviral disease model;
Encephalomyelitis;
CNS dysfunction;
Autonomic dysfunction;
Central fatigue;
Abnormal muscle fatigability;
Motor weakness;
Delayed restoration of muscle power;
Potential severe neurological disability.
58. FAILURE TO EXPLAIN CLEARLY THAT M.E. IS "NOT" CFS, ME/CFS OR SEID
This distinction should be prominent on the Association's public information.
It should say clearly, under this disease framework:
ROYAL FREE DISEASE / M.E.
=
SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE.
CFS
=
SYMPTOM-DEFINED SYNDROME.
ME/CFS
=
COMPOUND UMBRELLA TERM.
SEID
=
SYMPTOM-DEFINED NON-DIAGNOSTIC CONSTRUCT.
THESE ARE NOT INTERCHANGEABLE.
Failure to communicate this distinction allows patients, clinicians, researchers and policy-makers to assume equivalence that has not been demonstrated.
59. FAILURE TO DISTINGUISH CENTRAL FATIGUE FROM GENERALISED FATIGUE
CENTRAL FATIGUE ≠ (is NOT) GENERALISED FATIGUE.
60. FAILURE TO DISTINGUISH MOTOR WEAKNESS FROM PEM
CENTRAL FATIGUE
→ MUSCLE FATIGABILITY
→ MOTOR WEAKNESS
→ DELAYED RESTORATION OF MUSCLE POWER
is not synonymous with:
PEM.
61. FAILURE TO EXPLAIN AUTONOMIC AND GI MANIFESTATIONS
Public information should recognise:
Orthostatic dysfunction;
Heart-rate abnormalities;
Blood-pressure abnormalities;
Temperature dysregulation;
Sweating abnormalities;
Bladder dysfunction;
Gastroparesis;
Paralytic ileus;
Other intestinal dysmotility.
XII. PACE AND ACTION FOR M.E.
62. FAILURE TO PREVENT "CFS" RESEARCH BEING EXTRAPOLATED TO M.E.
Without demonstrated equivalence, findings from misdiagnosed CFS populations cannot automatically be treated as findings about Royal Free/Ramsay M.E.
This follows directly from the core disease distinction:
A SYMPTOM-DEFINED CFS COHORT
is not automatically
A SPECIFIC SUDDEN-ONSET ROYAL FREE/RAMSAY NEUROLOGICAL COHORT.
63. FAILURE TO EFFECTIVELY CHALLENGE ACTION FOR M.E.'S PACE INVOLVEMENT BEFORE THE TRIAL PROCEEDED
The ME Association later opposed PACE and GET.
The criticism is that it failed to defend the M.E. disease boundary strongly enough before and during the PACE era.
The basic objection should have been:
OXFORD CFS ≠ (is NOT) ROYAL FREE/RAMSAY M.E.
Therefore:
AN OXFORD-CFS TRIAL CANNOT ESTABLISH EFFICACY OR SAFETY FOR ROYAL FREE/RAMSAY M.E.
64. FAILURE TO PROTECT PATIENTS WITH ACTUAL NEUROLOGICAL OR INFECTIOUS DISEASE
Exercise therapy does not:
Eradicate enterovirus;
Treat encephalitis;
Treat encephalomyelitis;
Diagnose CNS infection;
Treat gastroparesis;
Treat paralytic ileus;
Repair neurological injury.
65. FAILURE TO HOLD ACTION FOR M.E. ADEQUATELY ACCOUNTABLE
Questions should have included:
Why was an M.E.-branded organisation involved with an Oxford-CFS trial?
What established equivalence to M.E.?
Who represented Royal Free/Ramsay patients?
Why should findings generated in a symptom-defined CFS population apply to a specific sudden-onset encephalomyelitic neurological disease?
XIII. MEDICAL LEADERSHIP - DR. CHARLES SHEPHERD AND DR. ABHIJIT CHAUDHURI
66. FAILURE OF MEDICAL LEADERSHIP DURING THE LONG SHEPHERD ERA
Dr. Charles Shepherd's long-running influence warrants scrutiny concerning:
Loss of a Ramsay-specific disease identity;
Promotion of "Encephalopathy";
Conflation of a specific neurological disease with symptom-defined populations;
Failure to secure onset diagnostics;
Failure to establish neurological/infectious pathways;
Failure to resolve enterovirus persistence;
Failure to prioritise antiviral development;
Failure to preserve the central-fatigue/motor-fatigability framework;
Acceptance of PEM-centred frameworks;
Inadequate recognition of severe autonomic/GI dysfunction;
Failure to guarantee Ramsay-patient governance;
Inadequate specialist services;
Public information.
Responsibility should not automatically be attributed solely to Dr. Shepherd.
Trustees and other relevant decision-makers also require examination.
67. WHAT QUALIFIED DR SHEPHERD TO DEFINE OR SPEAK FOR ROYAL FREE/RAMSAY M.E.?
Dr. Shepherd's institutional authority derives from medical training, his position and decades of involvement with the Association.
That is different from demonstrating that his own illness was Royal Free/Ramsay M.E.
His published illness followed chickenpox/varicella. Previously reported as Chickenpox Encephalitis.
That does not itself establish that he had the same disease as the Royal Free population.
The Association should therefore explain what disease-specific evidence and expertise justified his extensive influence over:
Nomenclature;
Disease definition;
Research priorities;
Medical information;
Clinical policy;
Patient representation.
68. ORGANISATIONAL AUTHORITY IS NOT DISEASE-SPECIFIC EXPERTISE
A long institutional position does not automatically establish specialist neurological, infectious-disease or virological authority.
It also does not establish authority to redefine a separately described patient population through later symptom-based criteria.
70. SHEPHERD'S NICE NG206 ROLE CREATES AN ADDITIONAL ACCOUNTABILITY QUESTION
Dr. Shepherd served on the NICE NG206 committee.
Yet NG206 does not require:
Sudden neurological onset;
Encephalomyelitis;
Documented enterovirus;
Objective acute CNS disease;
Acute viral detection;
A Ramsay-defined phenotype;
The central-fatigue → muscle-fatigability → motor-weakness framework.
Under this critique, NG206 represents a chronic symptom-defined framework rather than the specific sudden-onset neurological disease being described here.
Why was such a framework accepted for patients carrying the M.E. name?
71. FAILURE TO EXPLAIN THE LOSS OF DR. ABHIJIT CHAUDHURI AS A NEUROLOGICAL ADVISER
The Association should clarify:
Why did he resign after NG206 ?
Did he regard NG206 as appropriate for Royal Free/Ramsay M.E., or inappropriate ?
Did he regard a symptom-defined chronic framework as equivalent to the sudden-onset neurological disease he had advised upon?
Did disagreement within the MEA contribute to his departure?
72. NEED FOR AN INDEPENDENT REVIEW OF SHEPHERD-ERA MEDICAL POLICY
The review should examine:
Trustee minutes;
Medical-adviser correspondence;
Research-funding decisions;
Nomenclature decisions;
NICE submissions;
NG206 discussions;
Dr. Chaudhuri's departure;
Patient involvement;
Enterovirus policy;
Antiviral policy;
Public-information policy;
The basis on which symptom-defined CFS/ME-CFS/SEID populations came to be represented under the M.E. identity.
XIV. MISSION DRIFT, CHARITABLE PURPOSE AND TRUSTEE ACCOUNTABILITY
73. FAILURE TO PREVENT FUNDAMENTAL MISSION DRIFT
Under this critique:
ROYAL FREE/RAMSAY M.E.
SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE
↓
M.E.
↓
CFS
SYMPTOM-DEFINED SYNDROME
↓
ME/CFS
COMPOUND UMBRELLA
↓
IOM/SEID-INFLUENCED FRAMEWORK
SYMPTOM-DEFINED CONSTRUCT
↓
NICE NG206.
If these represent materially different populations, this is not merely evolving terminology.
It represents mission drift from a specific neurological disease population toward later symptom-defined beneficiary populations.
74. FAILURE TO ESTABLISH THAT THE NEW POPULATIONS WERE THE SAME BENEFICIARIES
The Association should demonstrate the scientific and governance basis on which broader populations came to be represented through the original M.E. identity.
The mere use of "ME/CFS" cannot establish equivalence.
A symptom-defined misdiagnosis cannot automatically establish membership of the original Royal Free/Ramsay disease population.
75. POSSIBLE CHANGE IN BENEFICIARY CLASS
If the effective beneficiary class changed from:
ROYAL FREE/RAMSAY M.E.
SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE
to
CFS
SYMPTOM-DEFINED POPULATION
to
ME/CFS
BROADER COMPOUND POPULATION
to
SEID/IOM-INFLUENCED POPULATIONS,
that should be tested against the charity's original governing purposes set out by Dr. Melvin Ramsay.
76. WAS "M.E." REDEFINED WHILE THE CHARITABLE OBJECTS REMAINED THE SAME?
If the wording remained "M.E." while its clinical meaning changed, the beneficiary population may have changed beneath an apparently unchanged charitable object.
This is particularly important if:
ORIGINAL M.E.
=
ROYAL FREE/RAMSAY SUDDEN-ONSET NEUROLOGICAL DISEASE
but
LATER INSTITUTIONAL M.E.
=
CFS / ME-CFS / SEID-STYLE SYMPTOM POPULATIONS.
That requires investigation.
77. FAILURE TO PROTECT THE ORIGINAL BENEFICIARY POPULATION FROM DISPLACEMENT
Potentially displaced priorities include:
Sudden-onset diagnostics;
CNS investigation;
Autonomic investigation;
GI dysmotility;
Enterovirus detection;
Neurological services;
Persistent infection;
Antiviral development;
Severe neurological disability;
M.E.-specific research.
78. FAILURE TO PROTECT RAMSAY RESEARCH FUNDING FROM MISSION DRIFT
An independent audit should establish:
Which populations received funding?
Which criteria were used?
Were they Royal Free/Ramsay-defined patients or symptom-defined CFS/ME-CFS/SEID populations?
What were donors told?
Were donations restricted?
Were restrictions followed?
79. NEED FOR A CHARITY-GOVERNANCE AUDIT
Obtain:
Historical constitutions/articles;
Objects clauses;
Charity Commission records;
Name changes;
Applications to amend purposes;
Approvals;
Trustee resolutions;
Annual reports;
Research-fund documents;
Restricted-fund documentation;
Medical-policy statements.
The audit should determine whether the organisation remained focused on the original disease population or progressively substituted later symptom-defined entities for it.
XV. MISREPRESENTATION OF THE ORIGINAL ROYAL FREE/RAMSAY COHORT
80. FAILURE TO REPRESENT THE ORIGINAL COHORT ACCURATELY
Under this framework, representing Royal Free/Ramsay patients; through CFS, ME/CFS or SEID-style constructs misrepresents:
Disease identity;
Aetiology;
Sudden onset;
CNS pathology;
Autonomic dysfunction;
Motor dysfunction;
Severity;
Clinical urgency;
Research priorities.
The central representational problem is that a:
SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE
can become represented publicly as a:
SYMPTOM-DEFINED CHRONIC FATIGUE / PEM POPULATION.
Under this framework, those are not equivalent.
81. FAILURE TO REPRESENT THE SERIOUSNESS OF CNS DISEASE
Brainstem encephalitis can cause severe permanent neurological disability and can be fatal.
Encephalomyelitis can likewise cause major neurological impairment and can, in severe circumstances, be life-threatening.
82. FAILURE TO ADVOCATE FOR EMERGENCY NEUROLOGICAL RECOGNITION
Sudden:
Cranial-nerve palsies;
Bulbar dysfunction;
Severe paresis;
Altered consciousness;
Autonomic instability;
Respiratory compromise;
Acute myelopathic abnormalities;
Encephalitic features
require urgent medical assessment.
83. FAILURE TO REPRESENT BRAINSTEM DISEASE
Brainstem pathology can affect:
Breathing;
Swallowing;
Speech;
Cranial nerves;
Autonomic regulation;
Heart rate;
Blood pressure;
Balance;
Eye movements;
Protective reflexes.
84. FAILURE TO REPRESENT SPINAL CORD DISEASE
Spinal cord pathology can affect:
Motor function;
Sensation;
Autonomic function;
Bladder/bowel function;
Mobility;
Respiratory function depending upon level;
Long-term disability.
85. FAILURE TO REPRESENT AUTONOMIC GI DISEASE
Autonomic/neurological disease can affect:
Gastric emptying;
Intestinal motility;
Bladder function;
Cardiovascular regulation;
Other visceral functions.
Gastroparesis, paralytic ileus and significant dysmotility should therefore be treated as medical manifestations requiring appropriate investigation.
86. THE ORIGINAL COHORT SHOULD HAVE BEEN RING-FENCED
The safeguard should have been:
DISTINCT RAMSAY/ROYAL FREE DEFINITION
+
EXPLICIT SEPARATION FROM CFS / ME-CFS / SEID
+
SEPARATE RESEARCH COHORTS
+
SEPARATE BIOBANKING
+
SEPARATE EPIDEMIOLOGY
+
APPROPRIATE CLINICAL PATHWAYS
+
DISEASE-SPECIFIC PUBLIC INFORMATION
+
DISEASE-SPECIFIC TREATMENT RESEARCH
+
TRANSPARENT FUNDING.
XVI. NEED FOR AN URGENT NEW NICE GUIDELINE AND NHS PATHWAY
87. NICE NG206 SHOULD NOT SUBSTITUTE FOR A ROYAL FREE/RAMSAY M.E. GUIDELINE
Under this critique, NG206 addresses a different diagnostic construct.
It is based on a chronic symptom-defined framework.
It therefore should not prevent creation of a separate guideline for the specific sudden-onset neurological disease described here.
88. AN URGENT NEW NICE GUIDELINE IS REQUIRED FOR ACTUAL M.E.
The proposed guideline should cover:
MYALGIC ENCEPHALOMYELITIS
(ROYAL FREE DISEASE /
ENTEROVIRAL ENCEPHALOMYELITIS)
under:
ATYPICAL POLIOMYELITIS.
89. THE NEW GUIDELINE SHOULD DISTINGUISH TWO PROPOSED PRESENTATIONS
ATYPICAL POLIOMYELITIS
01. MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS) / ASEPTIC MENINGITIS (ENTEROVIRAL MENINGOENCEPHALOMYELITIS)
02. ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME.
90. THE GUIDELINE SHOULD BEGIN AT ONSET, NOT MONTHS LATER
SUDDEN NEUROLOGICAL ILLNESS
↓
URGENT MEDICAL ASSESSMENT
↓
INFECTIOUS-DISEASE + NEUROLOGICAL INVESTIGATION
↓
VIRAL DETECTION
↓
ENTEROVIRUS IDENTIFICATION/SUBTYPING
↓
CSF WHERE CLINICALLY INDICATED
↓
BRAIN/SPINAL IMAGING WHERE INDICATED
↓
AUTONOMIC/CARDIAC/RESPIRATORY/GI INVESTIGATION
↓
LONGITUDINAL FOLLOW-UP
↓
VIRAL CLEARANCE OR PERSISTENCE
↓
NEUROLOGICAL OUTCOME
↓
DISEASE-MODIFYING/PATHOGEN-DIRECTED RESEARCH.
91. THE GUIDELINE MUST USE THE CORRECT MOTOR FRAMEWORK
CENTRAL FATIGUE
↓
ABNORMAL MUSCLE FATIGABILITY
↓
POST-EXERTIONAL MOTOR WEAKNESS
↓
DELAYED RESTORATION OF MUSCLE POWER.
NOT:
PEM.
92. THE GUIDELINE MUST RECOGNISE CNS/AUTONOMIC DISEASE WITHOUT GENERALISED FATIGUE
A patient can present with:
CNS dysfunction;
Brainstem abnormalities;
Motor dysfunction;
Cranial neuropathies;
Autonomic dysfunction;
Gastroparesis;
Paralytic ileus;
Other GI dysmotility;
Bladder dysfunction;
Cardiovascular autonomic abnormalities
without unexplained generalised fatigue being the dominant complaint.
93. THE GUIDELINE MUST RECOGNISE MEDICAL SEVERITY
It should include explicit red-flag pathways for:
Bulbar dysfunction;
Respiratory compromise;
Severe weakness;
Acute flaccid paralysis;
Cranial-nerve abnormalities;
Autonomic instability;
Severe dysphagia;
Gastroparesis with nutritional compromise;
Paralytic ileus;
Major neurological deterioration.
94. CENTRAL NICE DEMAND
For whichever of the proposed neurological presentations applies to the individual patient:
AN URGENT, SEPARATE NICE GUIDELINE AND NHS CLINICAL PATHWAY FOR ROYAL FREE/RAMSAY MYALGIC ENCEPHALOMYELITIS IS REQUIRED.
NICE NG206 should not be used as a substitute for this disease-specific pathway.
The distinction should be:
NICE NG206
=
CHRONIC SYMPTOM-DEFINED CFS / ME-CFS / IOM-SEID-INFLUENCED FRAMEWORK.
SEPARATE NEW NICE GUIDELINE
=
ROYAL FREE/RAMSAY : MYALGIC ENCEPHALOMYELITIS /
ENTEROVIRAL ENCEPHALOMYELITIS /
ATYPICAL POLIOMYELITIS.
XVII. CUMULATIVE ACCOUNTABILITY
95. THE CUMULATIVE PATTERN WARRANTS INDEPENDENT INVESTIGATION
Under this critique:
ROYAL FREE/RAMSAY M.E.
SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE
↓
ENCEPHALOMYELITIS WEAKENED
↓
ORIGINAL COHORT BLURRED
↓
M.E. CONFLATED WITH CFS
↓
ME/CFS NORMALISED
↓
SEID/IOM-INFLUENCED SYMPTOM FRAMEWORK ACCEPTED
↓
DISTINCTION BETWEEN DISEASE ENTITY AND SYMPTOM CONSTRUCT LOST
↓
CORRECT ATYPICAL POLIOMYELITIS TERMINOLOGY LOST
↓
GENERALISED FATIGUE BECOMES CENTRAL
↓
PEM REPLACES THE MOTOR FRAMEWORK
↓
SUDDEN CNS ONSET IS LOST
↓
AUTONOMIC DYSFUNCTION IS UNDER-REPRESENTED
↓
GI DYSMOTILITY IS UNDER-REPRESENTED
↓
ACUTE DIAGNOSTICS ARE NOT ESTABLISHED
↓
ENTEROVIRUS IS NOT MADE CENTRAL
↓
PERSISTENCE REMAINS UNRESOLVED
↓
ANTIVIRAL DEVELOPMENT IS NOT MADE CENTRAL
↓
SEVERELY AFFECTED PATIENTS REMAIN WITHOUT ADEQUATE SERVICES
↓
RAMSAY PATIENTS LACK GUARANTEED GOVERNANCE POWER
↓
RAMSAY-ASSOCIATED FUNDING IS NOT NECESSARILY RESTRICTED TO RAMSAY COHORTS
↓
POTENTIAL MISSION DRIFT
↓
POTENTIAL REPLACEMENT OF THE ORIGINAL BENEFICIARY CLASS
↓
POTENTIAL MISREPRESENTATION OF THE ORIGINAL ROYAL FREE/RAMSAY PATIENT POPULATION.
The cumulative effect can be investigated as possible institutional suppression or erasure of the Royal Free/Ramsay disease model.
XVIII. PROPOSED REFORM
96. RESTORE THE CORRECT DISEASE-SPECIFIC MISSION
Restore:
ATYPICAL POLIOMYELITIS
01. MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS) / ASEPTIC MENINGITIS (ENTEROVIRAL MENINGOENCEPHALOMYELITIS)
02. ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME.
Maintain explicitly:
ROYAL FREE DISEASE / M.E.
=
SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE.
CFS
=
SYMPTOM-DEFINED SYNDROME.
ME/CFS
=
COMPOUND UMBRELLA TERMINOLOGY.
SEID
=
SYMPTOM-DEFINED DIAGNOSTIC CONSTRUCT.
Therefore:
M.E. ≠ (is NOT) CFS.
M.E. ≠ (is NOT) ME/CFS.
M.E. ≠ (is NOT) SEID.
97. RESTORE DIRECT PATIENT GOVERNANCE
People with Ramsay-defined M.E. should have meaningful representation within:
Trustees/board;
Medical policy;
Scientific policy;
Research committees;
Grant decisions;
Ramsay Research Fund;
Clinical advocacy;
Public information;
Medical-adviser appointments.
Principle:
NOTHING ABOUT RAMSAY-DEFINED M.E. WITHOUT RAMSAY-DEFINED M.E. PATIENTS INVOLVED IN THE DECISION.
98. CONSIDER DR. WILLIAM WEIR AS A MEDICAL ADVISER
Consider Dr. William Weir as one potential Medical Adviser, particularly concerning the clinical and neurological presentation of Ramsay-defined M.E.
99. CONSIDER DR. JOHN CHIA AS A MEDICAL/SCIENTIFIC ADVISER
Consider Dr. John Chia particularly concerning:
Enterovirus infection;
Enterovirus-associated disease;
Viral persistence;
Tissue investigation;
Viral reservoirs;
Pathogen-directed research;
Antiviral development and evaluation.
100. CONSIDER JANE COLBY AS A PATRON
Consider Jane Colby, historically associated with Tymes Trust, as a potential Patron, recognising her longstanding advocacy concerning children and young people with M.E.
A Patron must not replace direct patient governance.
101. ESTABLISH MULTIDISCIPLINARY MEDICAL LEADERSHIP
Appropriate expertise should include:
Neurology;
Infectious diseases;
Clinical virology;
Enterovirus biology;
Neuropathology;
Neuromuscular medicine;
Cardiology;
Autonomic medicine;
Gastroenterology/GI motility;
Nutrition;
Immunology;
Severe neurological disability.
102. REFORM RESEARCH GOVERNANCE
Ramsay-defined patients should participate directly in determining:
What qualifies as M.E.-specific research;
Which diagnostic definitions are acceptable;
Which projects receive Ramsay funding;
How much goes to onset diagnostics;
How much goes to CNS/autonomic research;
How much goes to motor dysfunction;
How much goes to enterovirus;
How much goes to persistence;
How much goes to antivirals.
103. ESTABLISH PROSPECTIVE ONSET COHORTS
Follow:
ACUTE ENTEROVIRUS
↓
SUDDEN CNS DISEASE
↓
NEUROLOGICAL + AUTONOMIC INVESTIGATION
↓
CENTRAL FATIGUE
+
MUSCLE FATIGABILITY
+
MOTOR WEAKNESS
↓
VIRAL CLEARANCE OR PERSISTENCE
↓
LONG-TERM OUTCOME.
104. ESTABLISH APPROPRIATE SERVICES FOR SEVERE AUTONOMIC AND GI DISEASE
According to clinical need:
Autonomic medicine;
Gastroenterology;
GI motility services;
Gastric-emptying investigation;
Management of gastroparesis;
Management of paralytic ileus;
Specialist nutrition;
Enteral feeding;
Parenteral nutrition where medically necessary;
Inpatient care.
105. MAKE ENTEROVIRUS AND ANTIVIRAL RESEARCH CENTRAL
Establish:
Onset viral detection;
Subtyping;
Longitudinal virology;
Tissue-reservoir research;
Persistence studies;
Antiviral discovery;
Appropriately selected treatment trials.
106. AUDIT THE CHARITY AND RAMSAY RESEARCH FUND
Conduct independent:
Scientific audit;
Financial audit;
Governance audit;
Historical objects/beneficiary audit;
Research-cohort audit.
Determine whether the organisation and its funding remained directed toward the specific Royal Free/Ramsay neurological disease population it claimed to represent, or whether resources progressively shifted toward different symptom-defined populations.
FINAL REFORM MODEL
ATYPICAL POLIOMYELITIS
↓
01. MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS) / ASEPTIC MENINGITIS
(ENTEROVIRAL MENINGOENCEPHALOMYELITIS)
OR
02.
ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME
↓
SUDDEN NEUROLOGICAL ONSET
↓
URGENT NEUROLOGICAL + INFECTIOUS-DISEASE ASSESSMENT
↓
ENTEROVIRUS DETECTION AND SUBTYPING
↓
CNS + AUTONOMIC + MOTOR INVESTIGATION
↓
WHERE PRESENT:
GASTROPARESIS
+
PARALYTIC ILEUS
+
OTHER GI DYSMOTILITY
+
CARDIOVASCULAR AUTONOMIC DYSFUNCTION
+
BLADDER/AUTONOMIC DYSFUNCTION
↓
CENTRAL FATIGUE
↓
ABNORMAL MUSCLE FATIGABILITY
↓
POST-EXERTIONAL MOTOR WEAKNESS
↓
DELAYED RESTORATION OF MUSCLE POWER
↓
PROSPECTIVE M.E.-SPECIFIC COHORTS
↓
VIRAL CLEARANCE / PERSISTENCE RESEARCH
↓
TISSUE-RESERVOIR RESEARCH
↓
ANTI-ENTEROVIRUS DRUG DEVELOPMENT
↓
APPROPRIATE SPECIALIST AND HOSPITAL SERVICES
↓
PROTECTION OF THE MOST SEVERELY AFFECTED
↓
RAMSAY-SPECIFIC RESEARCH + TRANSPARENT FUNDING
↓
DR. WILLIAM WEIR
Potential Medical Adviser
+
DR. JOHN CHIA
Potential Medical/Scientific Adviser
+
JANE COLBY
Potential Patron
+
RAMSAY-DEFINED M.E. PATIENTS
Direct governance authority
↓
ACCOUNTABILITY TO THE ORIGINAL PATIENT POPULATION.
CENTRAL CONCLUSION
Under the premises of this critique, the alleged failure of the ME Association is not simply inadequate advocacy.
It is the progressive loss and potential misrepresentation of the specific Royal Free/Ramsay patient population from which the organisation derived its M.E. identity.
The defining distinction must remain explicit:
ROYAL FREE DISEASE / MYALGIC ENCEPHALOMYELITIS
=
A SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE.
CFS
=
A SYMPTOM-DEFINED SYNDROME.
ME/CFS
=
A COMPOUND UMBRELLA TERM.
SEID
=
A SYMPTOM-DEFINED NON-DIAGNOSTIC CONSTRUCT.
THESE ARE NOT INTERCHANGEABLE ENTITIES.
The terminology "ME/CFS" should therefore not be conflated with:
ROYAL FREE DISEASE;
MYALGIC ENCEPHALOMYELITIS;
ENTEROVIRAL ENCEPHALOMYELITIS;
ENTEROVIRAL MENINGOENCEPHALOMYELITIS;
or
ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME.
Under the proposed framework, the clinically clearer umbrella is:
ATYPICAL POLIOMYELITIS.
The disease framework is not:
UNEXPLAINED GENERALISED FATIGUE
+
PEM.
It is:
SUDDEN-ONSET ENTEROVIRAL NEUROLOGICAL DISEASE
with
CNS DYSFUNCTION
+
AUTONOMIC DYSFUNCTION
and the characteristic motor sequence:
CENTRAL FATIGUE
→ ABNORMAL MUSCLE FATIGABILITY
→ POST-EXERTIONAL MOTOR WEAKNESS
→ DELAYED RESTORATION OF MUSCLE POWER.
Autonomic disease can additionally produce major organ dysfunction, including gastroparesis, paralytic ileus and other gastrointestinal dysmotility.
Brainstem encephalitis and encephalomyelitis can produce permanent neurological disability and, in severe presentations, can be life-threatening.
Under this critique, replacing that specific neurological/infectious disease framework with later symptom-defined CFS, ME/CFS or SEID constructions potentially changes:
WHO HAS THE DISEASE;
WHAT THE DISEASE IS CALLED;
WHETHER A SPECIFIC DISEASE IS REPLACED BY A SYMPTOM-DEFINED SYNDROME;
WHAT PATHOLOGY IS INVESTIGATED;
WHEN THE PATIENT IS DIAGNOSED;
WHETHER THE PATIENT IS HOSPITALISED;
WHICH TESTS ARE PERFORMED;
WHICH SPECIALISTS BECOME INVOLVED;
WHICH RESEARCH COHORTS ARE CREATED;
WHAT RESEARCH IS FUNDED;
WHAT TREATMENTS ARE DEVELOPED;
AND WHICH PATIENT POPULATION THE CHARITY ACTUALLY REPRESENTS.
The failure to preserve the distinction between:
A SPECIFIC SUDDEN-ONSET NEUROLOGICAL DISEASE
and
LATER SYMPTOM-DEFINED CFS / ME-CFS / SEID ENTITIES
therefore sits at the centre of the alleged:
DIAGNOSTIC MISREPRESENTATION;
COHORT SUBSTITUTION;
RESEARCH MISCLASSIFICATION;
CLINICAL MISDIRECTION;
MISSION DRIFT;
FUNDING MISDIRECTION;
AND MISREPRESENTATION OF THE ORIGINAL ROYAL FREE/RAMSAY BENEFICIARY POPULATION.
Accordingly, under this framework, an urgent separate NICE guideline and NHS clinical pathway for actual Royal Free/Ramsay Myalgic Encephalomyelitis is required.
That guideline should be constructed around:
ATYPICAL POLIOMYELITIS
01. MYALGIC ENCEPHALOMYELITIS
(also known as ENTEROVIRAL ENCEPHALOMYELITIS) / ASEPTIC MENINGITIS
(ENTEROVIRAL MENINGOENCEPHALOMYELITIS)
02. ENTEROVIRAL POLIOMYELITIS-LIKE SYNDROME.
It should begin at sudden neurological onset, not after months of unexplained fatigue.
NICE NG206 should not be treated as a substitute for that disease-specific neurological and infectious-disease pathway.
And the ME Association should be required to explain how, when and on what scientific and governance basis a charity historically associated with a specific Royal Free/Ramsay neurological disease came to represent later CFS, ME/CFS and SEID-style symptom-defined populations under the same M.E. identity.
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