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Advances in Neurology and Neuroscience(AN)

ISSN: 2690-909X | DOI: 10.33140/AN

Impact Factor: 1.12

Narrative Case Study - (2026) Volume 9, Issue 4

Longitudinal Health Symptom, Treatment and Control Summary (2008-2026) A Longitudinal Synthesis of Symptom Burden, Autonomic Linkage, Intervention, Recovery and Present Level of Control

Bruce H. Knox *
 
Independent Scholar, Auckland, New Zealand
 
*Corresponding Author: Bruce H. Knox, Independent Scholar, Auckland, New Zealand

Received Date: Sep 21, 2026 / Accepted Date: Oct 16, 2026 / Published Date: Oct 28, 2026

Copyright: ©2026 Bruce H. Knox. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: Knox, B. H. (2026). Longitudinal Health Symptom, Treatment and Control Summary (2008–2026) A Longitudinal Synthesis of Symptom Burden, Autonomic Linkage, Intervention, Recovery and Present Level of Control. Adv Neur Sci, 9(4), 01-16.

Abstract

This document brings together 50 recorded health conditions or symptom complexes across the period 2008–2026. Its purpose is to show, in one longitudinal record, what occurred, how each problem may or may not relate physiologically to secondary autonomic dysfunction/MSAD, what treatment or management was used, what outcome followed, and the present level of control. The table is therefore both a chronology and a functional account of recovery, adaptation and continuing clinical burden. This is, fundamentally, a very personal medical log, arising from my own recordings, observations and continuing analysis of a complex health journey since 2008.

Purpose and Scope

This document brings together 50 recorded health conditions or symptom complexes across the period 2008–2026. Its purpose is to show, in one longitudinal record, what occurred, how each problem may or may not relate physiologically to secondary autonomic dysfunction/MSAD, what treatment or management was used, what outcome followed, and the present level of control. The table is therefore both a chronology and a functional account of recovery, adaptation and continuing clinical burden. This is, fundamentally, a very personal medical log, arising from my own recordings, observations and continuing analysis of a complex health journey since 2008. The account has been developed in dialogue with the medical team that has supported me, whose clinical assessments and care have helped validate its central observations, and it has also been tested against relevant findings reported in the medical literature. I wrote it primarily to help myself understand the sequence, interrelationships and changing significance of what has happened over nearly two decades. It is therefore offered with the understanding that it is personal, candid and deliberately honest—not as a substitute for individual medical advice, but as a carefully considered lived-experience record that may help others facing a similar situation gain a greater sense of confidence, context and understanding in making sense of their own journey.

What has been done

• Each row is anchored to a period and a two- or three-word symptom summary, allowing the reader to identify the issue immediately before reading the detailed explanation.

• Column 2 records the condition or symptom complex and then, in italics, evaluates the MSAD/autonomic linkage using four mutually exclusive categories: PROBABLE, POSSIBLE, INDIRECT or NO ASSOCIATION. The colour-coded word in each row identifies the linkage category immediately.

• The linkage analysis is based on recognised physiology, the documented timing and pattern of symptoms, and the cumulative autonomic-reserve framework developed through the author’s MSAD work. It is intended to express biological plausibility, not to claim that every symptom was caused by dysautonomia.

• Key sources are identified within the cells and hyperlinked so that the underlying reference material can be opened directly.

• Columns 3–5 then show management, observed outcome and a current status classification: Resolved (R), Under Control (UC), Under Control Watchlist (UCWL), or Not Under Control Watchlist (NUCWL).

Current Position at a Glance

50

46

4

92%

recorded entries

resolved or under control

not under control

resolved or controlled

The statistical summary records 11 resolved entries (22%), 26 under control (52%), 9 under control but retained on the watchlist (18%), and only 4 not under control and remaining on the watchlist (8%). Thus, 46 of 50 entries (92%) are either resolved or presently controlled, although some continue to require active monitoring. UC and UCWL together account for 35 entries (70%) that remain under active management or control.

A selection of musical presentation can be accessed in this flipbook. These lyrics capture much of the story outlined in the summary findings below.

How the Table Should Be Read

Method, interpretive framework and meaning of the status categories

• Longitudinal Method

The table uses a retrospective longitudinal synthesis. It follows the documented sequence of illness, procedures, symptoms, interventions and response over time rather than treating each problem as an isolated event. This makes it possible to distinguish conditions that preceded the major autonomic deterioration from symptoms that appeared, intensified or became more functionally important after the later cardiovascular events.

• Three-Hit Physiological Framework

The table is interpreted against a three-hit working model: Hit 1 is the late-2008 CHIKV illness, described in the clinical history at the time as the virus “attacking the heart”, followed by myocarditis and subsequent cardiovascular difficulties; Hit 2 is the ventricular perforation, cardiac tamponade and haemodynamic collapse during LVOT PVC ablation on 15 October 2021; Hit 3 is the same-day emergency sternotomy, cardiopulmonary bypass and ventricular repair. The model proposes that repeated viral-inflammatory, haemodynamic and major-surgical stress may have cumulatively reduced autonomic and physiological reserve. It is a biologically plausible explanatory framework, not proof of a single causal chain.

• How Autonomic Linkage is Expressed

Autonomic linkage status

Meaning in this table

PROBABLE

Recognised autonomic mechanism with a strong fit to the documented pattern.

POSSIBLE

Biologically plausible relationship, but the symptom is not specific to autonomic dysfunction.

INDIRECT

The condition may amplify symptom burden, reduce cardiovascular or physiological reserve, or complicate autonomic compensation without itself being an autonomic manifestation.

NO ASSOCIATION

No direct autonomic association is identified; the condition is retained as a separate structural, inflammatory, mechanical or other diagnosis. Any indirect reserve effect is described separately where relevant.

• Meaning of the Current Status

Code

Interpretation

Current total

R

Resolved

11 | 22%

UC

Under control

26 | 52%

UCWL

Under control, but retained on watchlist because significant care, specialist review or close monitoring remains necessary

9 | 18%

NUCWL

Not under control and retained on watchlist

4 | 8%

 

PROBABLE — 18 | 36%

POSSIBLE — 15 | 30%

INDIRECT — 13 | 26%

NO ASSOCIATION — 4 | 8%

• Overall Interpretation: MSAD as a Multisystem Package

Taken together, the linkage classifications show a coherent system-level pattern rather than a collection of 50 unrelated problems. Of the 50 recorded entries, 18 (36%) are PROBABLE, 15 (30%) are POSSIBLE, and 13 (26%) are INDIRECT. Only 4 (8%) are classified as NO ASSOCIATION. Thus, 46 of 50 entries (92%) have at least a probable, possible or indirect physiological relationship to the wider autonomic picture, while four are best retained as separate diagnoses. This does not mean that MSAD caused all 46 conditions; rather, it shows that autonomic dysfunction provides a plausible integrating framework for understanding how many of the symptoms arose, interacted, were amplified, or became harder to compensate for. In this synthesis, MSAD is therefore best understood as a package: an umbrella description of an autonomic nervous system whose automatic regulatory functions became dysregulated across several domains at the same time. The table documents strong or plausible autonomic involvement in blood-pressure and baroreflex control, heart-rate and vascular responses to standing and exertion, sweating and temperature regulation, gastrointestinal motility, bladder filling and emptying, pupillary responses, and the fatigue/cerebral-perfusion burden of upright activity. Other structural, inflammatory, cardiac or mechanical conditions sit around that core picture as indirect contributors because they can add physiological load, reduce reserve, or make autonomic compensation more difficult. The three-hit chronology offers a coherent temporal context for this cumulative loss of reserve, while remaining a working physiological model rather than proof of a single causal chain.

The positive conclusion is equally important. A dysregulated autonomic system is not necessarily a permanently failing system. Across this record there is substantial evidence of recovery, compensation, treatment response and learned management. Independently of the linkage classifications above, 46 of the 50 entries (92%) are now either resolved or under control, including those retained on the watchlist; only four entries (8%) remain classified as not under control. Taken as a whole, the longitudinal pattern is therefore most consistent with multifactorial secondary dysautonomia that has been extensive but increasingly contained: the system remains vulnerable and imperfectly regulated, but the dominant direction is toward adaptation, restored function and practical control rather than relentless deterioration.

Important interpretive limit: this remains a longitudinal single-case synthesis. The linkage categories describe physiological plausibility and interaction, not proof that autonomic dysfunction caused every recorded condition. Structural, inflammatory, medication-related and other diagnoses remain identified separately where appropriate.

Longitudinal Health Symptom, Treatment and Control Summary (2008 2026)

Highlighted entries are those identified from the table wording as involving significant ongoing care, specialist review, or close monitoring.

Status: R = Resolved | UC = Under control | UCWL = Under Control Watchlist | NUCWL = Not Under Control Watchlist Amber highlight = UCWL/NUCWL: [not] / under control, but requiring significant ongoing care, specialist review, or close monitoring

Autonomic-linkage colour key used below: PROBABLE = recognised autonomic mechanism with a strong fit to the documented pattern; POSSIBLE = biologically plausible but not specific; INDIRECT = may amplify burden, reduce physiological reserve or modify autonomic compensation; NO ASSOCIATION = no direct autonomic association identified and the condition is retained separately. These linkage categories express physiological plausibility, not proof of causation, and are separate from the R/ UC/UCWL/NUCWL clinical-control status in the final column.

Three-hit framework: Hit 1 = late-2008 CHIKV illness, described in this clinical history by the treating cardiologist as the virus 'attacking the heart', followed by myocarditis/cardiovascular dificulties; Hit 2 = ventricular perforation with cardiac tamponade and haemodynamic collapse during LVOT PVC ablation on 15 October 2021; Hit 3 = same-day emergency sternotomy, cardiopulmonary bypass and ventricular repair. The model proposes cumulative loss of autonomic/physiological reserve from repeated viral-inflammatory, haemodynamic and major-surgical stress. It is a working physiological hypothesis based on temporal sequence and biological plausibility, not proof of causation.

Period

Medical condition or symptom complex/how this is related to MSAD

Treatment or management approach

Outcome or level of control achieved

Status

2008

Urinary outlet obstruction

Prostate/urethral problems, later including urethral stricture and obstructed emptying

MSAD linkage (POSSIBLE): structural outlet disease is not autonomic, but bladder filling sensation, detrusor activity and coordinated emptying depend on autonomic pathways. In this history, urethral obstruction and possible autonomic bladder dysfunction can therefore coexist and compound incomplete emptying. Three-hit context: later autonomic bladder impairment may have been superimposed on pre-existing structural outlet disease, especially after Hits

2-3.

Key source: National Institute of Diabetes and Digestive and Kidney Diseases, “Autonomic  Neuropathy.”

Prostate surgery in 2008;

intermittent self-catheterisation; urethroplasty in 2019; another urethral procedure in November 2022

Structural repair and catheterisation provided management; later urinary emptying difficulties persisted.

UC

2008, late

Acute chikungunya—CHIKV: fever, rash, severe joint pain and profound fatigue. The clinical

Hospital

You survived

R

Acute

understanding at the time was that a virus was attacking your heart, with no clear prediction of

admission in April

the acute illness.

 

CHIKV

which way the outcome would go.

2009 with critical-

Persistent joint

 

illness

MSAD linkage (POSSIBLE): major viral illness can be followed by persistent autonomic

care monitoring

symptoms, fatigue

 

 

disturbance through post-viral inflammatory, immune and neural mechanisms. Within the

and supportive

and subsequent

 

 

cumulative-injury/autonomic-reserve framework developed in the MSAD work, CHIKV

management for

cardiovascular

 

 

is therefore a biologically plausible early 'hit', although the later dysautonomia cannot

the acute viral

difficulties became

 

 

be attributed to it alone. Three-hit context: this is Hit 1, the proposed initiating viral-

illness and cardiac

part of the longer

 

 

inflammatory/cardiac stressor in the model.

involvement

health journey.

 

 

Key source: National Institute of Neurological Disorders and Stroke, “Postural Tachycardia

 

 

 

 

Syndrome (POTS).”

 

 

 

2008

Persistent or recurrent joint pain following CHIKV

Ongoing symptom

Persistent joint pain

UC

onwards

MSAD linkage (INDIRECT): persistent post-CHIKV joint pain is not itself an autonomic sign,

monitoring,

remained part of

 

Persistent

but chronic pain and inflammatory stress can increase sympathetic load, reduce activity and

pacing and

the longer recovery;

 

joint pain

deconditioning reserve, and consume physiological reserve. It may therefore amplify MSAD

activity

pacing and activity

 

 

burden without being caused by MSAD. Three-hit context: persistent post-CHIKV pain added

adjustment during

adjustment

 

 

physiological load after Hit 1 and may have reduced later reserve.

recovery from

supported day-

 

 

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

CHIKV

to-day function,

 

 

 

 

with the degree

 

 

 

 

of resolution

 

 

 

 

remaining variable.

 

2009

Myocarditis, diagnosed at North Shore Hospital

Cardiology

Cardiac function

UC

Myocarditis

MSAD linkage (INDIRECT): myocarditis is a cardiac inflammatory injury rather than an

assessment,

stabilised

 

cardiac

autonomic diagnosis, but it can reduce cardiovascular reserve and increase the work required

cardiac monitoring

sufficiently

 

injury

of autonomic compensation. In a cumulative-injury model it is a biologically plausible

and continuing

for substantial

 

 

contributor to reduced reserve, not proof of autonomic causation. Three-hit context: post-Hit

management

professional

 

 

1 myocarditis represents an early documented cardiac injury within the cumulative-reserve

following the

activity to continue,

 

 

model.

myocarditis

although the

 

 

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

diagnosis

myocarditis-

 

 

 

 

specific

 

 

 

 

contribution to later

 

 

 

 

symptoms cannot

 

 

 

 

be isolated.

 

2009

Coronary artery disease requiring coronary stent placement

Cardiac stenting

Coronary stenting

UC

onwards

MSAD linkage (INDIRECT): coronary artery disease is a separate structural vascular

recorded in 2008

treated the

 

Coronary

disorder, but reduced cardiac/perfusion reserve and vasoactive treatment can materially limit

and March 2022;

identified arterial

 

artery

the body's ability to compensate for standing and exertion. It can therefore magnify autonomic

another account

disease; symptom-

 

disease

symptoms without being attributed to MSAD.

mentions 2010

specific benefit is

 

 

Key source: Juraschek et al., AHA Scientific Statement on orthostatic hypotension in adults

 

difficult to separate

 

 

with hypertension.

 

from the broader

 

 

 

 

cardiac history,

 

 

 

 

and the procedural

 

 

 

 

chronology varies

 

 

 

 

between accounts.

 

2009

onwards Persistent hypertension

Persistent hypertension, sometimes difficult to control

MSAD linkage (PROBABLE): blood-pressure stability depends heavily on baroreflex-mediated sympathetic and parasympathetic responses. Persistent hypertension alternating with orthostatic pressure falls is physiologically consistent with impaired baroreflex/autonomic

Spironolactone introduced; renal ablation for BP control in

A measure of control achieved, but substantial BP variability

NUCWL

 

regulation, while medication, renal and vascular factors may modify the pattern. Three-hit

October 2012;

continued. The

 

 

context: later worsening after Hits 2-3 is compatible with cumulative baroreflex/autonomic

later reported

contribution of each

 

 

vulnerability, without proving a single cause.

medicines

intervention is not

 

 

Key source: Juraschek et al., AHA Scientific Statement on orthostatic hypotension in adults

include losartan,

separately recorded.

 

 

with hypertension.

spironolactone

 

 

 

 

and Lasix

 

 

2009

Recurrent cutaneous irritation and rash

Identification

Management

UC

onwards

MSAD linkage (INDIRECT): rash is not a recognised core manifestation of dysautonomia.

and avoidance of

centred on avoiding

 

Recurrent

Inflammatory or medication-related skin disease can, however, increase systemic stress

suspected irritants

suspected triggers

 

skin rash

and autonomic demand, so it may add to overall MSAD burden while retaining a separate

or medication

and treating

 

 

dermatological explanation.

triggers, with

irritation when

 

 

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

skin-directed

present; the longer-

 

 

 

symptomatic care

term pattern of

 

 

 

as required

recurrence remains

 

 

 

 

unclear.

 

2011

Atrial fibrillation: abnormal heart rhythm

AF catheter

AF brought under

UC

Atrial

MSAD linkage (POSSIBLE): atrial fibrillation is an electrophysiological arrhythmia, but

ablation; Pradaxa

control and ceased

 

fibrillation

atrial rhythm is influenced by sympathetic-parasympathetic balance and autonomic reflexes.

also appears

to be the dominant

 

 

Autonomic dysregulation can therefore modify susceptibility or symptom expression, although

in your later

rhythm problem.

 

 

AF itself does not establish MSAD. Three-hit context: AF followed Hit 1; the timing is

medication history

Anticoagulation

 

 

compatible with altered cardiac-autonomic vulnerability but is not proof of causation.

 

served a separate

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

protective purpose.

 

2011 and later Reflux

oesophageal pain

Reflux, oesophageal or chest discomfort, nocturnal throat/oesophageal burning and pain MSAD linkage (POSSIBLE): vagal and enteric pathways coordinate oesophageal peristalsis, sphincter function and upper-GI motility. Reduced autonomic motor reserve can therefore worsen reflux, transit or swallowing symptoms, while EoE and other structural/inflammatory causes remain independently important.

GERD assessment and treatment; gastroscopy, acid monitoring and barium swallow;

Reflux reportedly

resolved after G-POEM; later inflammatory oesophageal

R

 

Key source: NIDDK, “Autonomic Neuropathy.”

later G-POEM

symptoms required

 

 

 

and EoE-directed

separate treatment.

 

 

 

treatment

 

 

2014 and

Severe hip joint disease requiring total hip replacement

Total hip

Both diseased

R

March

MSAD linkage (INDIRECT): hip disease is structurally musculoskeletal, not autonomic. Pain,

replacements

hip joints were

 

2021

reduced mobility and deconditioning nevertheless reduce the reserve available for upright

 

surgically replaced,

 

Severe hip

compensation and can amplify orthostatic intolerance, gait limitation and falls risk within a

 

providing structural

 

disease

multifactorial MSAD picture.

 

treatment and

 

 

Key source: Fedorowski et al., “Orthostatic Hypotension: Management of a Complex, But

 

supporting

 

 

Common, Medical Problem.”

 

mobility; the degree

 

 

 

 

of pain relief is

 

 

 

 

not separately

 

 

 

 

quantified.

 

2017

Falls, near-falls, gait instability and fall-related injuries, including broken bones

Hospital

The walking

NUCWL

onwards;

MSAD linkage (PROBABLE): documented orthostatic hypotension can directly produce

assessment when

stick, activity

 

severe

dizziness, visual narrowing, presyncope, instability and falls through reduced cerebral

required; walking

modification

 

episodes in

perfusion. Musculoskeletal, vestibular and balance factors may coexist, but the autonomic

stick; activity

and postural

 

2022 and

mechanism is physiologically strong where episodes track upright BP deterioration. Three-

modification and

management

 

2026

hit context: falls began before 2021, but more severe later episodes are compatible with

management

support safer

 

Falls gait

amplification after Hits 2-3.

of postural

participation,

 

instability

Key source: Fedorowski et al., “Orthostatic Hypotension: Management of a Complex, But

symptoms

although gait

 

 

Common, Medical Problem.”

 

instability and falls

 

 

 

 

risk persist.

 

2018

Recurrent or severe urinary infections, antibiotic resistance and sepsis reported in earlier

Antibiotic

Antibiotics and

UCWL

and after

history

treatment and

hospital care treated

 

procedures

MSAD linkage (POSSIBLE): autonomic bladder dysfunction can impair sensation and

hospital care

acute episodes, but

 

in 2021–

emptying, leaving residual urine that increases infection risk. Urethral obstruction and

 

recurrent infection,

 

2022

catheterisation provide additional non-autonomic pathways, so recurrent infection is plausibly

 

resistance and

 

Recurrent

the downstream result of interacting autonomic and structural factors.

 

the earlier sepsis

 

urinary

Key source: NIDDK, “Autonomic Neuropathy.”

 

history continued to

 

infections

 

 

complicate urinary

 

 

 

 

management.

 

2019–2021

Frequent premature ventricular contractions, reaching approximately 15,000 in 24 hours

LVOT PVC

PVC problem

R

Frequent

MSAD linkage (POSSIBLE): PVCs are an electrophysiological rhythm disorder rather than

ablation on 15

treated, but the

 

PVCs

a diagnostic sign of dysautonomia, but ventricular excitability and symptom perception are

October 2021

procedure caused

 

 

influenced by sympathetic-parasympathetic balance. Autonomic instability can therefore

 

ventricular

 

 

interact with the arrhythmia and with BP/HR regulation without being its sole cause. Three-

 

perforation and

 

 

hit context: PVCs preceded Hits 2-3; their ablation precipitated Hit 2, followed immediately

 

tamponade.

 

 

by Hit 3.

 

 

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

 

 

2019

Heat intolerance and difficulty regulating body temperature

Activity and

Temperature

UC

onwards;

MSAD linkage (PROBABLE): sweating, cutaneous vasodilation/vasoconstriction and heat

environmental

regulation became

 

worse after

dissipation are autonomically regulated. Heat intolerance and impaired temperature control

adaptation; pacing

more dependable

 

2021

therefore have a direct physiological route from autonomic dysfunction, although medication,

 

during recovery,

 

Heat

cardiac status and deconditioning can add to the burden. Three-hit context: pre-2021

 

although heat

 

intolerance

heat intolerance worsening after Hits 2-3 supports amplification of an existing autonomic

 

remains a stressor.

 

 

vulnerability.

 

 

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

 

 

2020

onwards; pronounced after 2021 Orthostatic hypotension

Orthostatic hypotension: dizziness, light-headedness, presyncope and occasional syncope on standing

MSAD linkage (PROBABLE): orthostatic hypotension is a cardinal manifestation of impaired autonomic cardiovascular compensation. Inadequate vasoconstriction and/or heart-rate adaptation on standing can reduce venous return and cerebral perfusion, producing the

documented dizziness, presyncope and occasional syncope; medication and volume status may

Fluids and salt as clinically directed; compression garments and abdominal support; positional

Greater practical control and ability to function; postural pressure falls remain a major limitation.

NUCWL

 

add secondary effects. Three-hit context: orthostatic symptoms pre-dated 2021 but became

adaptation; head-

 

 

 

pronounced after Hits 2-3, strongly supporting a cumulative-reserve interpretation.

of-bed elevation;

 

 

 

Key source: Juraschek et al., AHA Scientific Statement on orthostatic hypotension in adults

pacing and BP

 

 

 

with hypertension.

monitoring

 

 

2020–2021;

Gallbladder dysfunction

Gallbladder dysfunction

MSAD linkage (POSSIBLE): gallbladder emptying is influenced by vagal, sympathetic and enteric-neurohormonal control, so autonomic dysfunction can plausibly modify biliary motility. Gallbladder disease, however, has many independent causes and should not be attributed to MSAD without specific evidence.

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

Cholecystectomy reported in an earlier account

The gallbladder disorder was described as settled after cholecystectomy; the operation date differs between the available accounts.*

R

2020-21

Biliary tract dysfunction

Clinical

Biliary symptoms

UC

Biliary

MSAD linkage (POSSIBLE): biliary motility is partly under neural and neurohormonal

monitoring and

remained

 

tract

control, and broader autonomic GI dysmotility can alter coordinated digestive function. This

evaluation of

under clinical

 

dysfunction

gives a biologically plausible connection, but biliary tract disease remains nonspecific and

biliary symptoms,

evaluation and

 

 

requires its own explanation.

considered

were considered

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

separately from

separately from

 

 

 

the gallbladder

the gallbladder

 

 

 

disorder

disorder; a

 

 

 

 

distinct treatment

 

 

 

 

response cannot

 

 

 

 

be established

 

 

 

 

from the available

 

 

 

 

account.

 

2021

Altered or impaired sweating

Temperature

Sweating returned

R

onwards,

MSAD linkage (PROBABLE): sweat-gland output is controlled by autonomic sudomotor

regulation,

and became more

 

especially

pathways. Altered or impaired sweating is therefore a direct physiological autonomic

hydration, pacing

dependable.

 

Impaired

manifestation; later return of sweating is also consistent with selective recovery, compensation

and observation

 

 

sweating

or recalibration of autonomic function. Three-hit context: the post-Hits 2-3 timing strengthens

during autonomic

 

 

 

the fit with a broader multisystem autonomic deterioration.

recovery

 

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

 

 

2021

Delayed pupil response, light sensitivity and difficulty adapting between bright and dim

Softer, predictable

Provides practical

UC

onwards;

conditions

lighting and

accommodation;

 

described

MSAD linkage (PROBABLE): pupil size and light-dark adaptation depend on coordinated

environmental

complete resolution

 

in 2026

sympathetic and parasympathetic control. Delayed pupil response and impaired adaptation

adaptation

not reported.

 

Delayed

therefore have a direct autonomic pathway, although ocular or neurological causes should

 

 

 

pupillary

still be excluded. Three-hit context: this post-Hits 2-3 symptom fits the broader emergence of

 

 

 

response

autonomic signs after the 2021 insults.

 

 

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

 

 

2021

Cognitive fatigue, slower processing, difficulty finding words or making decisions under load

Pacing cognitive

Sustained

UC

onwards;

MSAD linkage (PROBABLE): cognitive slowing and fatigue can arise when orthostatic/

work, rest

thinking, writing

 

continuing

autonomic failure reduces cerebral perfusion and increases the metabolic effort needed

and assistive

and professional

 

in 2026

to maintain homeostasis. The close association with upright intolerance makes this

communication,

work regained;

 

Cognitive

physiologically plausible, while sleep, medication and other neurological factors remain

including LLM-

processing speed

 

fatigue

possible contributors. Three-hit context: prominence after Hits 2-3 is consistent with reduced

supported writing

and fatigue remain

 

 

cerebral-perfusion/autonomic reserve in the post-2021 phase.

 

limiting at times.

 

 

Key source: NINDS, “Postural Tachycardia Syndrome (POTS).”

 

 

 

2021–2026,

Trauma-related distress, fear, frustration, grief, emotional exhaustion and the burden of

Self-directed

Research, writing

UC

recurring

repeated setbacks

trauma processing

and musical

 

Trauma

MSAD linkage (INDIRECT): emotional stress activates sympathetic, cardiovascular and

through research,

expression provided

 

emotional

endocrine stress pathways and can temporarily consume autonomic reserve. It can therefore

explanatory

a framework

 

exhaustion

amplify an established dysautonomia; this is a bidirectional physiological interaction and

writing and

for processing

 

 

does not imply that the autonomic disorder is psychological in origin. Three-hit context: Hits

musical

repeated setbacks,

 

 

2-3 were themselves major physiological trauma; later emotional arousal can further tax

expression,

while pacing and

 

 

autonomic reserve.

together with

reduced demands

 

 

Key source: Goldstein, “Linking the Extended Autonomic System with the Homeostat Theory,”

pacing and

supported ongoing

 

 

2024.

adjustment of

adjustment.

 

 

 

daily demands

 

 

15 October

2021

Cardiac tamponade

Cardiac tamponade and haemodynamic collapse following ventricular perforation MSAD linkage (POSSIBLE): haemodynamic collapse, emergency sternotomy and cardiopulmonary bypass constitute major cardiovascular, inflammatory and neural stress.

Within the cumulative-injury/autonomic-reserve model, this event is a plausible major 'hit' capable of reducing autonomic reserve and preceding multisystem dysregulation, although causation cannot be proved from one case. Three-hit context: tamponade/haemodynamic collapse is Hit 2; the emergency sternotomy, CPB and ventricular repair constitute Hit 3. Key source: NINDS, “Postural Tachycardia Syndrome (POTS).”

Emergency sternotomy, cardiopulmonary bypass and ventricular repair

Life saved and immediate cardiac injury

repaired. Recovery was followed

by extensive multisystem difficulties.

R

October 2021

onwards Post-exertional fatigue

Severe fatigue, weakness, reduced endurance and slow recovery after exertion

MSAD linkage (PROBABLE): exertion requires rapid autonomic adjustment of heart rate, vascular tone and cerebral perfusion. Blunted or delayed compensation can produce weakness, breathlessness, fatigue and prolonged recovery; cardiac recovery and deconditioning may add to, but do not exclude, this autonomic mechanism. Three-hit context: onset immediately after Hits 2-3 gives this fatigue/endurance syndrome a particularly strong temporal relationship.

Key source: NINDS, “Postural Tachycardia Syndrome (POTS).”

Pacing, rest, protected exercise, recumbent cycling and treatment of individual cardiac, digestive and urinary problems

Meaningful recovery of activity and professional participation; fatigue and delayed recovery continue to fluctuate.

UC

2022–2026,

especially BP

regulation instability

Supine or resting hypertension alternating with low upright BP

MSAD linkage (PROBABLE): the combination of supine or resting hypertension with low upright BP is a recognised pattern of impaired autonomic/baroreflex control. Failure to buffer pressure appropriately in opposite postures provides a strong physiological link, while cardiovascular disease and medication can further shape the observed values. Three-hit

context: this post-Hits 2-3 BP pattern is a central expression of impaired baroreflex/autonomic reserve.

Key source: Juraschek et al., AHA Scientific Statement on orthostatic hypotension in adults with hypertension.

Specialist-directed medication management, home BP readings, head-of-bed elevation and adjustment of daily activity

Partial control; the coexistence of high and low pressures remains difficult to manage.

NUCWL

2022–2023,

Inadequate heart-rate response to standing or exertion, with breathlessness and exercise

Cardiology

Gradual

UC

especially

intolerance

review, heart-rate

improvement:

 

Blunted

MSAD linkage (PROBABLE): heart-rate adaptation to standing and exercise is partly

and symptom

exercise HR

 

heart-rate

autonomically mediated. A blunted chronotropic response with breathlessness and exercise

monitoring,

reportedly rose

 

response

intolerance therefore fits impaired autonomic cardiac regulation within the broader MSAD

graded activity

from rarely

 

 

pattern. Three-hit context: post-Hits 2-3 chronotropic limitation is compatible with worsened

within tolerance,

exceeding about 70

 

 

autonomic cardiac responsiveness.

and pacing to

bpm to around 100

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

limit exertional

during walking and

 

 

 

breathlessness

approximately 120

 

 

 

 

with greater effort

 

 

 

 

by late 2025.

 

2022–2024;

Autonomic storms: abrupt widespread physiological disturbance and exhaustion

Blood-pressure

Storms ceased

UC

later

MSAD linkage (POSSIBLE): abrupt multisystem episodes involving cardiovascular,

management,

or markedly

 

intermittent

thermoregulatory, gastrointestinal or exhaustion symptoms are physiologically compatible

pacing, trigger

diminished during

 

episodes

with unstable autonomic signalling and an exaggerated homeostatic stress response.

reduction, self-

2024–2026.

 

Autonomic

'Autonomic storm' remains a descriptive term rather than a separate diagnosis. Three-hit

monitoring and

Improvement

 

storms

context: emergence after Hits 2-3 fits a temporarily unstable, low-reserve autonomic system.

recovery during

cannot be attributed

 

 

Key source: Goldstein, “Linking the Extended Autonomic System with the Homeostat Theory,”

episodes

to one intervention

 

 

2024.

 

alone.

 

2022–2024,

Delayed gastric emptying/gastroparesis: early fullness, nausea, bloating and difficulty moving

Gastrointestinal

Improved gastric

UC

especially

food through the stomach

investigations;

emptying and

 

Delayed

MSAD linkage (PROBABLE): gastric emptying depends substantially on vagal, enteric

smaller meals;

digestive function;

 

gastric

and pyloric coordination. Autonomic neuropathy can slow gastric transit and produce

G-POEM in 2024

meaningful

 

emptying

gastroparesis, making the documented delayed emptying a recognised GI-autonomic

to address pyloric

improvement in

 

 

manifestation, while medication and local gastric factors may coexist. Three-hit context:

resistance

quality of life.

 

 

clinically important gastroparesis emerged after Hits 2-3, matching the broader post-2021

 

 

 

 

GI-autonomic deterioration.

 

 

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

 

 

2022

diagnosis;

Pancreatic exocrine insufficiency, impairing digestion

MSAD linkage (INDIRECT): the exocrine pancreas is densely regulated by parasympathetic and sympathetic pathways, so autonomic dysfunction can plausibly alter digestive secretion and gut-pancreatic coordination. Established pancreatic exocrine insuficiency nevertheless requires its own pancreatic explanation; within MSAD it may further reduce nutritional and physiological reserve.

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

Creon with meals

Digestion improved and pancreatic insufficiency brought under practical control with ongoing enzyme support.

UC

treatment

 

 

from 2023

 

 

Pancreatic

 

 

insuficiency

 

 

2022

onwards Constipation evacuation difficulty

Constipation and difficult evacuation

MSAD linkage (PROBABLE): autonomic and enteric pathways regulate colonic propulsion, rectal sensation and internal-sphincter behaviour. Dysfunction can therefore contribute to constipation and dificult evacuation; pelvic-floor, medication and structural mechanisms may coexist, especially where outlet relaxation is impaired. Three-hit context: post-Hits 2-3 onset fits the wider post-2021 pattern of enteric/autonomic dysmotility.

Key source: NIDDK, “Autonomic Neuropathy.”

Hydration, soluble fibre in earlier accounts, and Microlax when required

A measure of bowel control achieved; continued bowel management remained necessary.

UC

2022

onwards Dry eyes

Acute dry eyes

MSAD linkage (POSSIBLE): lacrimal secretion and ocular-surface homeostasis are influenced by autonomic parasympathetic and sympathetic pathways. Dry eyes can therefore form part of autonomic dysfunction, although local ocular-surface disease, medication and environmental factors are common alternative or additional causes. Three-hit context: post-Hits 2-3 timing is compatible with multisystem autonomic involvement but remains nonspecific.

Key source: NIDDK, “Autonomic Neuropathy.”

Prescribed eye drops following University

of Auckland Optometry Clinic assessment

Prescription eye drops provided a defined treatment pathway following optometry assessment;

the extent and durability of symptom relief are not quantified.

UC

2022

Muscle tightening and dystonic episodes occurring with autonomic disturbance

Pacing, postural

Pacing, gentle

UC

Muscle

MSAD linkage (POSSIBLE): dystonia or muscle tightening is not a core autonomic sign,

and autonomic

mobility and

 

dystonic

but sympathetic surges, pain, altered perfusion and heightened physiological arousal can

symptom

autonomic

 

episodes

trigger or intensify abnormal muscle contraction. A primary neurological or musculoskeletal

management,

management

 

 

explanation must remain in consideration. Three-hit context: post-Hits 2-3 timing makes

gentle mobility,

provided a practical

 

 

autonomic surges or altered perfusion plausible amplifiers, not proven causes.

and monitoring of

framework for

 

 

Key source: Goldstein, “Linking the Extended Autonomic System with the Homeostat Theory,”

muscle-tightening

episodes; their

 

 

2024.

episodes

frequency, severity

 

 

 

 

and response

 

 

 

 

remain under

 

 

 

 

observation.

 

2023

Colonic polyps

Four colonic polyps identified during colonoscopic investigation

MSAD linkage (NO ASSOCIATION): colonic polyps are structural mucosal lesions and are not explained by autonomic dysfunction. Their importance is gastrointestinal surveillance rather than evidence for MSAD.

Key source: NIDDK, “Autonomic Neuropathy.”

Colonoscopy and removal of four polyps

Polyps removed; a separate effect on bowel symptoms is not recorded.

R

2024, during oesophageal treatment Oesophageal medication irritation

Oesophageal irritation associated in your observations with taking Pradaxa

MSAD linkage (INDIRECT): medication-associated mucosal irritation is not autonomic, but impaired oesophageal motility or clearance could prolong local exposure and magnify symptoms. The observed relationship to Pradaxa remains clinical observation rather than

proof of an autonomic cause. Three-hit context: post-Hits 2-3 dysmotility could plausibly have reduced oesophageal clearance and amplified a medication-related injury.

Key source: NIDDK, “Autonomic Neuropathy.”

Taking the medicine with food, as you reported

Irritation reportedly settled. The proposed inflammatory

mechanism remains an interpretation.

R

2024

Altered taste

Altered taste

MSAD linkage (INDIRECT): taste is not a defining autonomic function, but autonomic control

Observation of taste changes,

Taste changes were managed through

UC

 

of salivary secretion and oral perfusion can influence the environment needed for normal taste

review of possible

observation,

 

 

perception. Medication, oral and gastrointestinal causes remain more direct alternatives, so

medication or

review of possible

 

 

the MSAD connection is biologically plausible but weak.

gastrointestinal

contributors and

 

 

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

contributors, and

dietary adaptation;

 

 

 

dietary adaptation

the subsequent

 

 

 

as needed

course remains

 

 

 

 

uncertain.

 

2025

recurrences;

Eosinophilic oesophagitis: swallowing difficulty, oesophageal discomfort and recurrent attacks MSAD linkage (INDIRECT): EoE is an inflammatory oesophageal disease, but autonomic/ enteric dysmotility can reduce oesophageal motor reserve while EoE reduces structural-mechanical reserve. The combined loss of reserve can plausibly lower the threshold for dysphagia or food-impaction symptoms without making MSAD the cause of EoE. Three-

hit context: EoE remains independent, but post-Hits 2-3 dysmotility may have reduced oesophageal functional reserve.

Key source: NIDDK, “Autonomic Neuropathy.”

Jorveza/ budesonide, followed at times by swallowed Flixotide/ fluticasone

Symptoms brought under control.

Approximately eight weeks without treatment or flare were reported

in 2026; later recurrence again required Jorveza.

UCWL

clinically

 

active after

 

G-POEM

 

Eosinophilic

 

oesophagitis

 

2025/26

During

Attacks associated in your observations with dog exposure

MSAD linkage (INDIRECT): an environmental or allergic trigger is not an autonomic phenomenon, but inflammatory activation can increase sympathetic and homeostatic load and transiently reduce available physiological reserve. The dog-exposure association remains observational and does not establish either allergy or autonomic causation.

Key source: Goldstein, “Linking the Extended Autonomic System with the Homeostat Theory,” 2024.

Grooming and bathing the dog; modifying close interaction

You reported elimination of that apparent trigger. This records your experience without establishing an allergy mechanism.

R

recurrent

 

EoE

 

symptoms

 

Suspected

 

allergic

 

trigger

 

2026

Post-meal exhaustion or “crash”, particularly about two hours after dinner

Smaller, more

Used to reduce

UC

Post-meal

MSAD linkage (PROBABLE): after a meal, blood is redistributed to the splanchnic

frequent meals;

the burden of

 

exhaustion

circulation and healthy compensation requires increased vascular resistance and appropriate

pacing around

eating; the evening

 

 

cardiac responses. When autonomic compensation is limited, this can produce postprandial

meals

crash remains a

 

 

hypotension, cerebral hypoperfusion and a delayed energy 'crash'; meal size and GI disease

 

vulnerability. Its

 

 

may intensify the effect. Three-hit context: this late post-Hits 2-3 symptom has a strong

 

separate treatment

 

 

physiological route through impaired splanchnic vascular compensation.

 

response is not

 

 

Key source: NINDS, “Postural Tachycardia Syndrome (POTS).”

 

quantified.

 

2026

Fluctuating focus or blurred vision; visual fatigue during reading, screens and conversation

Screen breaks,

Helps organise

UC

Blurred

MSAD linkage (PROBABLE): blurred or narrowed vision can result from reduced cerebral

pacing visual

visual demands;

 

vision

and ocular perfusion during inadequate autonomic BP compensation. Refractive, ocular-

work and

symptoms remain

 

fatigue

surface and neurological causes remain possible, but the physiological link is strong when

managing lighting

variable.

 

 

symptoms accompany upright pressure falls. Three-hit context: the post-Hits 2-3 timing is

 

 

 

 

most meaningful when visual symptoms track upright BP/perfusion deterioration.

 

 

 

 

Key source: NINDS, “Postural Tachycardia Syndrome (POTS).”

 

 

 

2026

Visual motion sensitivity, disorientation in busy surroundings and night-vision difficulty

Choosing

Practical

UC

Visual

MSAD linkage (POSSIBLE): autonomic pupillary dysfunction can impair light-dark

environments

management

 

motion

adaptation, while orthostatic cerebral hypoperfusion can worsen visual disorientation

carefully and

documented;

 

sensitivity

and motion sensitivity. Vestibular and ophthalmic disorders remain important alternative

adapting lighting

specific

 

 

explanations, so the association is plausible rather than specific. Three-hit context: these later

 

improvement in

 

 

symptoms are compatible with post-Hits 2-3 pupillary and cerebral-perfusion vulnerability.

 

night vision not

 

 

Key source: NINDS, “Postural Tachycardia Syndrome (POTS).”

 

recorded.

 

2026

Reduced hearing acuity requiring audiological assessment

Audiology and

Audiological

UC

Reduced

MSAD linkage (INDIRECT): hearing loss is not a recognised defining manifestation of MSAD

hearing-aid care

review established

 

hearing

and requires independent audiological assessment. Autonomic regulation of vascular tone and

discussed in your

a pathway for

 

 

systemic BP can influence inner-ear perfusion, providing a biological route for interaction,

history

hearing-aid support;

 

 

but there is insuficient evidence to attribute this hearing loss to dysautonomia.

 

the fitting status

 

 

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

 

and functional

 

 

 

 

benefit are not

 

 

 

 

yet clear from the

 

 

 

 

available history.

 

2026

Reduced vocal strength and endurance during sustained conversation

Voice

Voice conservation,

UC

Reduced

MSAD linkage (INDIRECT): sustained speech depends on respiratory endurance, perfusion

conservation,

hydration and

 

vocal

and energy reserve. Autonomic-related fatigue, breathlessness or reduced cardiovascular

pacing of

paced conversation

 

endurance

compensation can therefore limit vocal endurance, while laryngeal, pulmonary and age-

conversation,

support continued

 

 

related causes remain separate possibilities. Three-hit context: late post-Hits 2-3 voice fatigue

hydration and rest

communication,

 

 

may reflect reduced whole-body cardiovascular/autonomic reserve.

between periods

although vocal

 

 

Key source: NINDS, “Postural Tachycardia Syndrome (POTS).”

of speaking

strength and

 

 

 

 

endurance remain

 

 

 

 

limited during

 

 

 

 

sustained use.

 

2026,

especially Delayed walking deterioration

Delayed deterioration during walking: head pressure, light-headedness, visual narrowing and substantial BP falls after approximately 15–30 minutes or longer

MSAD linkage (PROBABLE): delayed deterioration during sustained upright walking, with head pressure, visual narrowing and measured BP falls, strongly fits failure of autonomic

vascular compensation and progressive cerebral hypoperfusion. Relative preservation of

Compression, hydration and salt as directed; pacing; walking stick; supported

Recumbent cycling remains comparatively preserved.

Sustained upright

UCWL

 

recumbent cycling further supports an orthostatic rather than purely muscular exercise

or recumbent

walking continues

 

 

limitation. Three-hit context: this is a strong late post-Hits 2-3 expression of limited autonomic

exercise

to be restricted.

 

 

vascular reserve under sustained gravitational stress.

 

 

 

 

Key source: Fedorowski et al., “Orthostatic Hypotension: Management of a Complex, But

 

 

 

 

Common, Medical Problem.”

 

 

 

2026,

Urinary hesitancy, incomplete emptying and retention

Tamsulosin,

SPC restored

UCWL

progressing

MSAD linkage (PROBABLE): bladder filling sensation, detrusor contraction, sphincter

morning/

dependable

 

Urinary

coordination and emptying are autonomically regulated. Neurogenic/autonomic dysfunction

evening self-

drainage and

 

retention

can therefore cause hesitancy and retention, while established urethral disease and medication

catheterisation,

brought the

 

 

provide concurrent structural or pharmacological contributors. Three-hit context: post-Hits

then suprapubic

immediate

 

 

2-3 progression supports autonomic bladder impairment superimposed on longstanding

catheter—SPC

emptying problem

 

 

structural urethral disease.

 

under practical

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

control.

 

2026; after

Slower healing and longer recovery from tissue injury

Surgical repair

Healing continues,

UCWL

surgery/

MSAD linkage (POSSIBLE): delayed healing is not a standard diagnostic feature of

where required,

but more slowly.

 

injury

dysautonomia, but autonomic disturbance can plausibly affect regional perfusion,

wound/catheter

No specific

 

Slow tissue

inflammatory signalling, stress responses and the physiological resources available for repair.

care, time and

treatment restoring

 

healing

The MSAD work therefore treats this as a hypothesis of reduced repair reserve, not established

careful pacing

repair speed is

 

 

causation. Three-hit context: the cumulative Hits 1-3 underpin the reduced-repair-reserve

 

documented.

 

 

hypothesis, while that relationship remains unproven.

 

 

 

 

Key source: Goldstein, “Linking the Extended Autonomic System with the Homeostat Theory,”

 

 

 

 

2024.

 

 

 

6

Accidental SPC loss after tubing was cut and the balloon deflated; tract subsequently closed

Attempted

Initial reinsertion

R

September

MSAD linkage (NO ASSOCIATION): accidental SPC loss and tract closure were mechanical

reinsertion and

unsuccessful; later

 

2026

complications. The autonomic relevance lies upstream: neurogenic or mixed-mechanism

subsequent

accounts describe

 

Accidental

bladder dysfunction may have contributed to the need for catheter drainage, but it did not

urological/catheter

functioning

 

SPC loss

cause the tubing/tract event itself.

management

SPC drainage.

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

Exact restoration

 

 

 

 

procedure needs

 

 

 

 

recording.

 

September

Generalised night sweating, exhaustion and a prolonged response following emotional triggers

Recovery over

Physical, cognitive

UC

2026

MSAD linkage (PROBABLE): sweating is directly autonomically controlled and emotional

several days;

and emotional

 

Night

triggers activate sympathetic stress pathways. Generalised sweating followed by prolonged

ongoing pacing

function improved

 

sweating

exhaustion is therefore physiologically compatible with dysregulated autonomic arousal,

and monitoring

markedly by

 

exhaustion

although infection, endocrine and medication causes must remain excluded. Three-hit context:

 

14 September;

 

 

this late post-Hits 2-3 episode is consistent with prolonged recovery from sympathetic/

 

subsequent triggers

 

 

sudomotor activation.

 

were better

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

contained.

 

September

Bright-red urinary bleeding, particularly as the bladder filled

Free drainage

You observed

UCWL

2026

MSAD linkage (NO ASSOCIATION): visible haematuria is not a recognised autonomic

through the

urine clearing or

 

Urinary

manifestation and requires independent urological assessment. Autonomic retention, bladder

SPC leg bag;

bleeding reducing

 

bleeding

overdistension and catheter dependence may create the mechanical context in which bleeding

urological review

with continuous

 

 

occurs, but they should not be assumed to be the bleeding source.

and planned

drainage. Persistent

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

investigations

or recurrent

 

 

 

 

bleeding was not

 

 

 

 

fully resolved in the

 

 

 

 

original account.

 

September

Bladder spasms and urethral leakage/incontinence despite SPC

Maintaining

Maintaining free

UCWL

2026

MSAD linkage (PROBABLE): autonomic bladder dysfunction can disturb storage pressure,

unobstructed

SPC drainage

 

Bladder

detrusor activity and coordinated emptying, producing urgency, leakage or spasm-like

SPC drainage,

supports bladder

 

spasms

symptoms. Catheter irritation, blockage or local bladder pathology can provoke the same

catheter review

emptying, while

 

leakage

symptoms, so autonomic and mechanical mechanisms can reasonably coexist. Three-hit

and urological

spasms and

 

 

context: post-Hits 2-3 autonomic bladder vulnerability and SPC irritation provide plausible

assessment of

urethral leakage

 

 

simultaneous mechanisms.

bladder spasms

remain active

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

and urethral

issues requiring

 

 

 

leakage

catheter review

 

 

 

 

and urological

 

 

 

 

assessment.

 

September

New bowel-outlet difficulty: urge preserved, stool apparently reaching the rectum, repeated

Existing bowel

Existing bowel

UCWL

2026,

attempts, incomplete emptying and a sense that the outlet would not relax

support, including

support provided

 

after SPC

MSAD linkage (POSSIBLE): autonomic/enteric dysfunction can alter colonic propulsion,

Microlax;

incomplete relief,

 

placement

rectal sensation and internal-sphincter coordination, while non-relaxation of the external

investigation and

and the new outlet

 

Bowel

outlet points to pelvic-floor recruitment. The change after SPC placement supports a

development of

difficulty remained

 

outlet

biologically plausible bladder-bowel interaction hypothesis, but the SPC-to-outlet pathway

a bladder–bowel

under investigation;

 

dysfunction

remains unproven. Three-hit context: this late post-Hits 2-3 problem arose after GI and

hypothesis

a relationship to

 

 

bladder dysautonomia were already established, supporting systems interaction.

 

SPC-related pelvic-

 

 

Key source: NIDDK, “Autonomic Neuropathy.”

 

floor recruitment

 

 

 

 

remains a working

 

 

 

 

hypothesis.

 

September

Incisional hernia/bulge near the SPC site

Photographic

Photographic

UCWL

2026

MSAD linkage (NO ASSOCIATION): an incisional hernia is a structural surgical

monitoring,

comparison and

 

Incisional

complication and should not be labelled an autonomic manifestation. Within the reduced-

comparison over

clinical assessment

 

hernia

repair-reserve hypothesis, autonomic dysregulation could theoretically influence perfusion

time and clinical

support monitoring

 

bulge

and recovery capacity, but this remains an indirect hypothesis rather than an explanation for

assessment of the

of the bulge; the

 

 

the hernia itself. Three-hit context: the hernia is not caused by the model; any link is indirect

bulge near the

need for hernia-

 

 

through the reduced-repair-reserve hypothesis.

SPC site

specific treatment

 

 

Key source: Blitshteyn, “Dysautonomia: a common comorbidity of systemic disease,” 2025.

 

remains to be

 

 

 

 

determined.

 

Statistical Summary of Recorded Health Entries

Measure

Number

% of all entries

Total entries

50

100.0%

Resolved (R)

11

22.0%

Under control (UC)

26

52.0%

Under Control Watchlist (UCWL)

9

18.0%

Not Under Control Watchlist (NUCWL)

4

8.0%

Interpretation: of 50 recorded entries, 11 are resolved (R: 22.0%), 26 are under control (UC: 52.0%), 9 are under control but remain on the watchlist (UCWL: 18.0%), and 4 are not under control and remain on the watchlist (NUCWL: 8.0%). These four categories are mutually exclusive and together account for 100% of entries. UC and UCWL together represent 35 of 50 entries (70.0%) that are currently controlled or actively managed.

Additional Reading

Issue(s) covered

Additional background reading

Urethral stricture, obstructed emptying, urinary retention

American Urological Association: Urethral Stricture Disease Guideline (2023 amendment)

National Institute of Diabetes and Digestive and Kidney Diseases: Autonomic Neuropathy

Acute chikungunya and persistent post-CHIKV joint pain

Goupil and Mores: Review of chikungunya virus-induced arthralgia de Moraes et al.: Long-term arthralgia after chikungunya

Myocarditis and cardiac recovery

American College of Cardiology: Diagnosis and management of myocarditis

American Heart Association: Myocarditis overview

Coronary artery disease, hypertension and orthostatic hypotension

Juraschek et al.: Orthostatic Hypotension in Adults With Hypertension—American Heart Association Scientific Statement Magkas et al.: Orthostatic hypotension—from pathophysiology to clinical applications

Atrial fibrillation and autonomic regulation

Vandenberk et al.: Autonomic nervous system in atrial fibrillation Qin et al.: Cardiac autonomic nervous system and atrial fibrillation

Reflux, oesophageal discomfort and swallowing symptoms

NIDDK: Autonomic Neuropathy—digestive-system manifestations

Hip disease, gait instability, falls and fall-related injury

New Zealand Falls Prevention Toolkit for Clinicians Detecting postural hypotension and falls risk

Urinary infections, catheter-associated infection and antibiotic resistance

EAUN: Catheter complications and catheter-associated urinary tract infection

Premature ventricular contractions and autonomic–arrhythmic interaction

Autonomic nervous system modulation in arrhythmias

Heat intolerance, sweating disturbance and temperature regulation

Mayo Clinic: Autonomic neuropathy symptoms and causes NIDDK: Autonomic Neuropathy—sweating and temperature regulation

Orthostatic hypotension, presyncope, syncope and delayed deterioration while walking

Merck Manual: Orthostatic Hypotension

Torabi et al.: Classical and delayed orthostatic hypotension Cerebral blood flow in orthostatic intolerance

Gallbladder and biliary-tract dysfunction

Richmond: Biliary dyskinesia—controversies, diagnosis and management

American College of Surgeons: Biliary dyskinesia management

Pupillary delay, light sensitivity and impaired dark adaptation

Mayo Clinic: Autonomic neuropathy and sluggish pupil response

Cognitive fatigue, slower processing, exercise intolerance and post-exertional weakness

Cerebral blood flow in orthostatic intolerance

Merck Manual: Orthostatic intolerance symptoms and mechanisms

Emotional triggers, autonomic arousal and multisystem symptom exacerbation

Cardiovascular autonomic dysfunction and clinical guidance

Cardiac tamponade, ventricular perforation and complications of catheter ablation

American College of Cardiology: Procedure-related complications of catheter ablation

Major complications after catheter ablation of cardiac arrhythmias

Supine hypertension alternating with low upright blood pressure

Hypertension and orthostatic hypotension: a challenging balance European hypertension guidance and cardiovascular autonomic dysfunction

Blunted heart-rate response to standing or exertion

Mayo Clinic: Autonomic neuropathy and exercise intolerance

Autonomic storms and abrupt widespread physiological disturbance

Autonomic dysfunction affecting several organ systems

Gastroparesis, delayed gastric emptying and G-POEM

American Gastroenterological Association: Management of gastroparesis

AGA Clinical Practice Update on G-POEM

Pancreatic exocrine insufficiency and pancreatic enzyme replacement

AGA: Evaluation and management of exocrine pancreatic insufficiency

Constipation, difficult evacuation and bowel-outlet dysfunction

AGA: Evaluation and management of constipation

AGA–ACG guideline: Pharmacological management of chronic idiopathic constipation

Dry eyes and autonomic–ocular-surface interaction

Kaido et al.: Autonomic nerve activity in dry eye with reduced tear stability

Autonomic nervous activity and unstable tear-film dry eye

Muscle tightening and dystonic episodes

Multisystem manifestations of autonomic dysfunction

Colonic polyps and post-polypectomy surveillance

US Multi-Society Task Force: Follow-up after colonoscopy and polypectomy

Medication-associated oesophageal irritation

American College of Gastroenterology: Eosinophilic oesophagitis guideline summary

Altered taste

Mayo Clinic: Autonomic neuropathy symptoms and differential contributors

Eosinophilic oesophagitis, dysphagia and swallowed topical steroids

American College of Gastroenterology: Updated eosinophilic oesophagitis guideline

ACG Clinical Guideline: Diagnosis and management of eosinophilic oesophagitis

Environmental or allergic triggers associated with oesophageal attacks

ACG: Eosinophilic oesophagitis diagnosis, treatment and monitoring

Post-meal exhaustion and postprandial orthostatic symptoms

Merck Manual: Meals as an aggravating factor in orthostatic hypotension

Blurred vision, visual narrowing, visual fatigue and cerebral hypoperfusion

Hypocapnia and cerebral hypoperfusion in orthostatic intolerance Cerebral blood flow in orthostatic intolerance

Visual motion sensitivity, disorientation and night-vision difficulty

Orthostatic intolerance and disequilibrium

Mayo Clinic: Autonomic neuropathy and light–dark adaptation

Reduced hearing acuity and increased communication load

Autonomic dysfunction as a multisystem condition

Reduced vocal strength and conversational endurance

Merck Manual: Fatigue, breathlessness and orthostatic intolerance

Neurogenic or mixed-mechanism bladder dysfunction

NIDDK: Autonomic neuropathy and bladder dysfunction Managing a suprapubic catheter

Slow tissue healing and prolonged recovery

Mayo Clinic: Autonomic neuropathy, circulation and systemic contributors

SPC loss, tract closure and catheter replacement

British Association of Urological Surgeons: Suprapubic catheter practice guidelines

Management after suprapubic catheter insertion

Night sweating and prolonged episodes after triggers

BMJ: Patients who report night sweats Persistent night sweats: Diagnostic evaluation

Visible urinary bleeding/haematuria

AUA/SUFU Guideline: Evaluation of haematuria

Bladder spasms, leakage and catheter complications

EAUN: Catheter complications

Clinical guidance: Bladder spasm and suprapubic catheter management

Incisional hernia or bulge near the SPC site

European Hernia Society: Midline incisional hernia guidelines