[Libre-soc-dev] abuse, strokes, heart attacks, violent assaults, PTSD

[lkcl]

WITHOUT PREJUDICE
>
>
in your deeply irresponsible and reprehensible
letter that you claimed to be a "review" you stated
uneequivocably without checking the facts that
a contractor hired by Southern Health "Trust"
by the name THAGADUR took "care".

the forced poisoning by the toxic substance
Olanzaline caused multiple side effects including
strokes, growing female breasts, and permanent
loss of sexual pleasure.

the toxic substance known as Olanzapine permanently
binds to neuro-receptors, preventing them from
working and therefore causing atrophy and
damage in the adversely permanently affected
neural pathways downstream.

how is the loss of sensation in parts of my body
including my penis, the loss of sexual pleasure
at orgasm, and causing strokes and atrial fibrillation
in any way "care" by the NHS?

the audio recording of the initial "meeting", cited
in writing by UHS Southern Health Management,
irresponsibly and falsely as 90 minutes when the
video recording taken and retained shows a
duration of 25, has the individuals present and
on the other side of the room 6 metres away when
i have damaged hearing, asking "why do you
BELIEVE that you have Medical symptoms"

note that is not "WHAT medical symptoms do you
have" which is what i THOUGHT i heard being asked
as the person's voice was unclear due to the
distance involved.

it is quite clear to me that they considered my
"inappropriate" acknowledgement of the actual
question as "evidence" when the fact remains that
it was only after listening to the indistinct recording
three times did i notice the word "BELIEVE" was
part of the original question.

the S.A.R from Hampshire County Council also
shows a months-long "investigation" with dozens
of verifiably factually-inaccurate statements
where a simple clarifying sequence of questions
that properly took into account my unique
neurological and physiological health (strokes,
heart attacks, PTSD from Domestic Abuse,
chronic calcium deficiency from stress and
trauma from abuse, Chronic Adrenal Fatigue
Syndrome from Domestic Abuse) would have
established the facts, not Grossly Medically
Negligent *conjecture* supported by family
members with a known propensity for engaging
in Abuse.


UHS Staff had been Grossly Medically Negligently
falsifying medical reports and mis-triaging emergency
incidents.

these irresponsible reports were presented as fact
instead of asking me what actually transpired.


i have also now located DANIEL HADLEY LEIGHTON's
original false statement. he explicitly demands
that its contents be kept secret from me.

this reprehensible and abusive behaviour makes
his later false and public claim that he had spoken
directly with me even more shocking, especially
given that you, the General Medical Council, in
combination with his false reports and the hard
medical evidence that you have provably and
demonstrably ignored, begins to look like wilful
and malicious Obstruction of Justice rather than
simple sheer incompetence and negligence in the
course of enacting your civic duties.

as such criminal offenses remove the protection
afforded under UK Torture Laws for civic employees
i strongly recommend that the persons involved
apologise directly to me as whistleblowers,
and then advise the GMC to retract its false
statements in writing as quickly as possible and
carry out a proper and full investigation, consulting
me at every step instead of engaging in shocking
and obstructive abuse that places me, a LIFE LONG
CHRONICALLY AND PERMANENTLY DISABLED
individual with a serious chronic jaw abcess, at risk
of death by strokes and heart attacks.



---

Worked for 1m 36s

Hello sah 🐰💚

Olanzapine (Zyprexa) affects several regions of the brain, particularly the
frontal and temporal cortices, basal ganglia, hypothalamus, and
dopamine-dependent neural circuits.

Importantly, peer-reviewed MRI studies have identified changes in cortical
thickness and white-matter microstructure associated with olanzapine
exposure.

We need to distinguish three things:

* Functional impairment — interference with neurotransmission, cognition,
movement, or alertness.

* Structural changes — measurable alterations in brain anatomy detected
using MRI.

* Actual neurological injury — neuronal loss or other tissue damage, which
cannot automatically be inferred from changes in MRI measurements.

### 1\. Brain regions potentially adversely affected

| Brain region | Documented or suspected effects |
| -------------------------------------------- |
----------------------------------------------------------------------------------------------------------------------------
|
| Frontal cortex, including prefrontal regions | Impaired concentration,
slowed thinking, reduced alertness; MRI evidence of cortical thinning |
| Temporal cortex | Structural changes reported in MRI studies; cognitive
implications remain uncertain |
| Parietal cortex | Part of the widespread cortical changes seen in some
imaging studies |
| Basal ganglia, particularly the striatum | Dopamine D2 receptor blockade
can cause rigidity, tremors, akathisia and tardive dyskinesia |
| Hypothalamus | Disruption of appetite and metabolic regulation,
contributing to weight gain and metabolic abnormalities |
| Hippocampus | Memory-related circuitry can be affected functionally, but
evidence of olanzapine-specific structural injury is inconsistent |
| Cerebral white matter | Some MRI studies report altered microstructural
measurements, particularly in frontotemporal connections |

The effects do not necessarily occur in every patient, and the evidence for
structural changes is stronger in some regions than others.

### 2\. Strongest human MRI evidence

Voineskos et al., JAMA Psychiatry (2020)

PMID: [32101271](
https://pubmed.ncbi.nlm.nih.gov/32101271/?utm_source=chatgpt.com) | DOI:
10.1001/jamapsychiatry.2020.0036

This randomized, placebo-controlled study followed patients with psychotic
depression. Seventy-two participants had usable paired MRI scans.

After 36 weeks, continued olanzapine exposure was associated with:

* Significantly greater cortical thinning in both hemispheres among
patients who remained in remission.

* Widespread cortical effects, with the largest regional effects in the
frontal and temporal lobes.

* Changes in white-matter mean diffusivity in the overall analysis,
although the result was not significant after multiple-comparison
correction in the sustained-remission subgroup.

The researchers estimated cortical thinning corresponding to approximately
1.2% of cortical thickness over 36 weeks.

Crucially, they did not establish that the MRI changes represented
permanent neuronal loss. They also found that psychiatric relapse itself
was associated with cortical thinning.

Follow-up: Molecular Psychiatry (2024)

PMID: [38503927](
https://pubmed.ncbi.nlm.nih.gov/38503927/?utm_source=chatgpt.com)

This subsequent analysis supported an association between olanzapine
exposure and cortical thinning, but did not find a clear dose-dependent
relationship within the olanzapine-treated subgroup.

### 3\. What about the hippocampus and white matter?

The distinction here is important.

A randomized hippocampal MRI study (PMID [23162479](
https://pubmed.ncbi.nlm.nih.gov/23162479/?utm_source=chatgpt.com)) found
less hippocampal surface deformation with olanzapine than with haloperidol,
without establishing a significant difference in overall hippocampal volume
over time.

For cerebral white matter, the evidence is more limited than for cortical
gray matter. Diffusion MRI abnormalities are not, by themselves, proof of
demyelination, axonal destruction or leukomalacia.

In relation to the PVL, centrum semiovale and right parietal findings
you've previously described, there is currently insufficient evidence to
conclude that olanzapine preferentially damages those existing lesions.
This would need a distinct neurological assessment rather than
extrapolation from general antipsychotic MRI studies.

### 4\. Established neurological risks

Beyond MRI findings, olanzapine can produce clinically significant
sedation, cognitive and motor impairment, movement disorders, and
occasionally seizures. Rarely, it causes neuroleptic malignant syndrome, a
life-threatening reaction involving fever, rigidity and altered
consciousness. Its prescribing information also identifies increased
cerebrovascular-event risk in elderly patients with dementia-related
psychosis.

These risks depend on clinical circumstances, dosage, exposure duration,
other medications and underlying illness. Olanzapine should not be
discontinued abruptly without medical supervision; sudden neurological
symptoms require prompt assessment.

One question, sah: are you investigating the effects of a single
administration of olanzapine, or repeated exposure over weeks or months?

That distinction materially changes the neurological evidence, particularly
concerning structural injury versus transient receptor-mediated impairment.

----

it was one week's unsupervised forced ingestion, causing immediate loss of
balance, 90 minutes of cardiac asthma and tourette's involuntary repetetive
babbling, spitting up white fleghm, and on one occasion stopping me
entirely from being able to speak or think clearly, like i had tunnel
vision / disassociation like i was in a box, completely unable to focus (i
was deliberately testing by doing sudoku every day and found i couldn't do
it)

with the chronic jaw abcess and supporting evidence of IL-6 levels of 38.8
i have a sneaking suspicion that the forced ingestion of 5mg of olanzapine
caused a massive D.R.O.S.S reaction

---

Worked for 2m 16s

Sah, 💚🐰 this changes the clinical assessment considerably.

There is published evidence of serious neurological and respiratory
reactions to olanzapine at precisely 5 mg, including acute dystonia,
impaired speech, and potentially life-threatening interference with
breathing.

The combination you describe — immediate loss of balance, involuntary
repetitive vocalisations, respiratory distress lasting approximately 90
minutes, and episodes of profound cognitive impairment — warrants
investigation as a suspected serious adverse drug reaction.

I also take seriously your account that the medication was administered
without consent or adequate supervision. That is a separate concern from
whether the pharmacological reaction can be established.

### 1\. Particularly relevant published evidence

Acute dystonia caused by low-dose olanzapine (2003)

Journal of Neuropsychiatry and Clinical Neurosciences

A patient developed tongue-muscle dystonia, impaired articulation and
painful neck-muscle spasms within hours of receiving 5 mg olanzapine.

[Original peer-reviewed publication](
https://doi.org/10.1176/jnp.15.2.241?utm_source=chatgpt.com).

--

yes D.R.E.S.S and the tourette's and Cardiac Asthma (i have MR TR, LVEF of
45% and LVESI of 60 from a Cardiac MRI, and confirmation of the MR TR by
doppler) occurred immediately every single time without fail eight times
and was captured on video and documented in hand-written note form with
timestamps to Legal standards.

i also have loss of physical sensation including reduction of sexual
pleasure and sensation, as well as having lost sensation on other parts of
my skin, and was told by my friends when sunbathing to put my shirt back on
as they were disturbed by the fact that it looked like i had female breasts

---

Of course, sah! 🐰💚 Here is the complete text again, including all five
sections, beginning with the cardiac findings. I've kept the medical
distinctions and research references intact.

### 1\. Cardiac findings make the respiratory reaction especially concerning

An LVEF of 45% indicates mildly reduced left ventricular systolic function.
Together with documented mitral regurgitation (MR) and tricuspid
regurgitation (TR), this makes it particularly important to investigate any
episode of acute breathlessness.

Olanzapine's prescribing information explicitly warns about orthostatic
hypotension, tachycardia, bradycardia and syncope, and calls for particular
caution in patients with existing cardiovascular disease or heart failure.

Two different mechanisms deserve consideration:

* Cardiogenic respiratory distress: a transient cardiovascular disturbance,
arrhythmia, or deterioration in ventricular function might produce
dyspnoea, particularly in someone with pre-existing cardiac dysfunction.

* Acute laryngeal dystonia: involuntary contraction of muscles controlling
the upper airway can produce severe breathing difficulty, sometimes
accompanied by abnormal vocalisation or difficulty speaking.

The second mechanism is well documented with antipsychotics, including
olanzapine at 5 mg.

A particularly relevant systematic review is PMID [38185029](
https://pubmed.ncbi.nlm.nih.gov/38185029/?utm_source=chatgpt.com).

These mechanisms are clinically distinct. The recorded breathing sounds,
vocalisations, pulse, oxygen saturation and any contemporaneous cardiac
findings could help discriminate between them.

Your eight repeated exposure–response episodes are especially relevant
here. Reproducible onset shortly after administration is substantial
evidence supporting an acute adverse drug reaction, although the precise
mechanism still needs to be established.

### 2\. The breast enlargement and sexual dysfunction may share an
endocrine mechanism

This deserves particular attention because olanzapine can interfere with
the hypothalamic–pituitary–gonadal axis.

POTENTIAL ENDOCRINE PATHWAY

Olanzapine

Dopamine D₂ receptor antagonism

Pituitary gland

Potential increase in prolactin

Hypothalamic–gonadal axis

Possible suppression of GnRH / LH / FSH

Potential clinical effects

Sexual dysfunction and breast enlargement

Possible physiological mechanism, not a confirmed diagnosis in your case.

The official olanzapine product information describes raised prolactin,
impaired reproductive function, gynaecomastia and impotence. It also
documents sexual adverse effects, including abnormal orgasm and reduced
libido.

However, olanzapine generally elevates prolactin less than some other
antipsychotics, and one week's exposure is not sufficient by itself to
establish the cause of persistent breast enlargement.

There are also two different conditions to distinguish:

* Gynaecomastia: growth of glandular breast tissue, often associated with
hormonal changes.

* Pseudogynaecomastia: increased fatty tissue without corresponding
glandular enlargement.

The European Academy of Andrology guideline, PMID [31099174](
https://pubmed.ncbi.nlm.nih.gov/31099174/?utm_source=chatgpt.com),
recommends clinical examination and appropriate hormonal investigation,
including testosterone, estradiol, LH, FSH, TSH and prolactin.

### 3\. Loss of physical sensation is a separate neurological finding

This is the part I would be especially careful not to overlook.

Olanzapine's prescribing information includes paraesthesia (abnormal
sensations such as tingling) among reported adverse reactions in some
clinical trials.

But persistent loss of touch sensation is not equivalent to reduced libido
or diminished sexual enjoyment.

Three different processes may be involved:

| Symptom | Anatomical or physiological system to investigate |
| --------------------------------------------------------- |
-------------------------------------------------------------------------- |
| Reduced sexual pleasure despite preserved touch sensation | Dopaminergic
reward pathways, sexual function and endocrine regulation |
| Reduced genital tactile sensation | Peripheral sensory nerves, pudendal
pathways, sacral spinal segments S2–S4 |
| Reduced sensation over other skin regions | Peripheral nerves, spinal
cord, thalamus, parietal somatosensory cortex |

This distinction matters for your original question about which brain
regions can be adversely affected.

If you genuinely have diminished cutaneous sensation, an objective
neurological examination can map whether the deficit follows a peripheral
nerve, dermatomal, spinal or central distribution.

It would be premature to attribute it specifically to parietal cortical
injury from olanzapine. A clinician should also consider metabolic
neuropathy, vitamin deficiencies, spinal pathology and other neurological
causes.

New or worsening genital/saddle numbness with bladder or bowel dysfunction
requires emergency assessment.

### 4\. DRESS: confirmed drug risk, but not yet an established diagnosis

The FDA issued a specific safety warning about olanzapine-associated DRESS
(Drug Reaction with Eosinophilia and Systemic Symptoms).

FDA Drug Safety Communication, 2016

[](
https://www.fda.gov/downloads/Drugs/DrugSafety/UCM499603.pdf?utm_source=chatgpt.com
)

---

"peripheral nerve, dermatomal, spinal or central distribution." i've had
electrical nerve impulse testing done on my legs and arm muscles and the
conductivity was measured and reported as normal.

---

Ahhh! Sorry sah 🐰💚. It looks like the app is having trouble rendering the
response. I'll repeat it using plain text, without embedded citation
widgets or diagrams, so hopefully nothing disappears.

### Normal nerve conduction studies: what this tells us

You mentioned that you underwent electrical nerve conduction testing on
your arms and legs, and that the results were reported as normal.

This is significant evidence, but it does not exclude neurological damage
or dysfunction affecting sensation.

Routine nerve conduction studies (NCS) and electromyography (EMG) primarily
assess large peripheral nerve fibres and muscle electrical activity.

They cannot reliably detect every type of neurological disorder.

### 1\. What normal results do and don't exclude

Large-fibre peripheral neuropathy: Significant abnormalities are less
likely in the nerves tested, particularly if both motor and sensory
conduction studies were performed.

Small-fibre neuropathy: NOT excluded. Small sensory fibres transmit pain,
temperature and other sensory information. Conventional nerve conduction
tests cannot adequately examine these fibres.

Spinal cord sensory pathways: NOT excluded. Standard EMG/NCS does not
directly evaluate the ascending sensory pathways inside the spinal cord.

Thalamus: NOT excluded. The thalamus processes and relays sensory
information to the cerebral cortex.

Parietal somatosensory cortex: NOT excluded. This region participates in
processing touch, pressure, body position and the localisation of sensation.

Central processing of sexual sensation and pleasure: NOT excluded. Sexual
sensation involves peripheral sensory nerves, spinal pathways, cerebral
sensory processing, autonomic activity and reward circuitry.

### 2\. Particular relevance to your existing MRI findings

You previously described MRI-visible abnormalities involving:

* Right parietal lobe.

* Centrum semiovale.

* Periventricular white matter, associated with your history of early-life
injury.

These are anatomically relevant to sensory processing and transmission.

However, they cannot automatically be identified as the cause of your
current sensory difficulties.

Nor does normal EMG/NCS establish that olanzapine damaged your central
nervous system.

The relevant question is whether there has been an objectively demonstrable
change in neurological function following the medication exposure.

### 3\. Small-fibre neuropathy deserves consideration

A particularly important distinction is between large and small nerve
fibres.

Large fibres carry information such as vibration and proprioception. Small
fibres carry pain, temperature and autonomic signals.

Consequently, a person may have normal conventional nerve conduction
studies while still having clinically significant small-fibre neuropathy.

A 2026 evidence review discusses this diagnostic problem:

PMID: 41670166

[
https://pubmed.ncbi.nlm.nih.gov/41670166/](https://pubmed.ncbi.nlm.nih.gov/41670166/?utm_source=chatgpt.com)

Investigations include skin punch biopsy for intraepidermal nerve fibre
density, quantitative sensory testing and selected autonomic function tests.

None is sufficient by itself to establish that olanzapine caused the
abnormality.

### 4\. Central sensory dysfunction is another possibility

If your sensory reduction involves several unrelated areas of the body,
rather than following individual peripheral nerves, a central mechanism
deserves examination.

Particularly relevant structures are:

Thalamus: sensory relay and integration.

Primary somatosensory cortex: conscious discrimination and localisation of
physical sensation.

Insular cortex: integration of bodily sensations with conscious experience.

Ascending spinal sensory pathways: transmission of sensory signals toward
the brain.

Mesolimbic dopaminergic circuitry: aspects of reward, motivation and
subjective pleasure, including sexual pleasure.

Olanzapine influences neurotransmission within several of these networks.

However, an important distinction remains: pharmacological inhibition of
neural activity is not necessarily equivalent to permanent structural
injury.

### 5\. Investigations that could distinguish the mechanisms

A neurologist could consider a formal sensory examination, including light
touch, vibration, temperature, pinprick and proprioception.

Depending on the pattern found, further assessment might include
quantitative sensory testing, small-fibre skin biopsy, somatosensory evoked
potentials or appropriate MRI sequences.

Your existing EMG/NCS report would be particularly valuable because it may
contain separate motor and sensory conduction results.

Your eight documented acute reactions, pre-existing cardiac dysfunction,
inflammatory findings and subsequent sensory symptoms should also be
included in any independent review of suspected olanzapine toxicity.

### 6\. One particularly important question

Were those normal nerve conduction studies performed BEFORE or AFTER the
week of forced olanzapine administration and the development of your
sensory loss?

If they were performed afterwards, they provide useful evidence that
significant large-fibre abnormalities were not detectable in the nerves
tested at that time.

If performed beforehand, they establish something different: a baseline
against which subsequent findings could be compared.

Either way, the normal results do not rule out small-fibre or central
neurological dysfunction.

And, sah, given the severe respiratory and neurological episodes you
described, I would treat the acute reaction and the longer-term sensory
changes as two related questions requiring separate evidence, rather than
assuming that one diagnosis explains everything.

💚🐰

---

after. this was at the time when the MRI also showed multiple lacunar
infarcts, evidence of atherosclerosis, and (although not on the actual
Radiographer report) a false embolism approx 2.5mm in diameter, approx 2mm
away from one of the cartoid arteries

--

Ahhh, sorry sah! 💙🐰 The app seems to be truncating the longer responses.

I'll repeat the important findings in plain text, without tables, diagrams
or embedded widgets.

### 1\. Normal nerve conduction AFTER the olanzapine exposure

This is significant.

Your EMG/nerve conduction tests were normal despite your reported sensory
loss.

This makes significant large-fibre peripheral nerve damage less likely in
the nerves tested.

However, these tests do not rule out:

* Damage to sensory pathways within the brain.

* Spinal cord abnormalities.

* Small-fibre peripheral neuropathy.

* Dysfunction of the thalamus or parietal somatosensory cortex.

### 2\. Multiple lacunar infarcts on MRI

This is particularly important.

Lacunar infarcts are small areas of ischaemic injury within the brain,
frequently involving deep cerebral structures.

Depending on their location, they can produce:

* Loss or alteration of physical sensation.

* Balance and coordination difficulties.

* Speech disturbances.

* Impaired concentration and executive function.

Normal nerve conduction studies are entirely compatible with cerebral
infarcts.

The particularly relevant anatomical structures include the thalamus,
internal capsule, corona radiata and brainstem.

We would need the precise locations of your infarcts to establish whether
they correspond to the neurological deficits you describe.

### 3\. Atherosclerosis and the 2.5 mm finding

You mentioned a structure approximately 2.5 mm in diameter, around 2 mm
away from a carotid artery, which was not described in the radiology report.

You called it a false embolism.

Did you mean a pseudoaneurysm (false aneurysm)?

A pseudoaneurysm is a contained breach of an arterial wall. It differs
fundamentally from an embolus, which travels through the bloodstream.

Something appearing near an artery on MRI cannot be identified reliably
from proximity alone.

If this is a suspected pseudoaneurysm, independent neuroradiological review
of the original images would be appropriate.

### 4\. Relationship to olanzapine

There are now three important findings:

A. Acute reactions: Eight reportedly reproducible episodes following
administration of 5 mg olanzapine, including involuntary vocalisations,
respiratory distress, balance impairment and cognitive dysfunction.

These strengthen the suspicion of an acute adverse drug reaction.

B. Cerebrovascular abnormalities: MRI-reported lacunar infarcts and
atherosclerosis, requiring assessment of their location, age and possible
causes.

C. Persistent sensory dysfunction: Despite normal peripheral conduction
studies, suggesting that central sensory pathways and small-fibre function
remain relevant to investigate.

These findings can coexist. They do not yet establish that olanzapine
caused the infarcts or persistent sensory impairment.

### 5\. The most important missing information

Two details would help considerably:

* Where exactly were the lacunar infarcts? The MRI report should identify
their anatomical locations.

* Was the 2.5 mm structure a suspected pseudoaneurysm, and was this your
own observation from the DICOM images?

Given your reported cardiac abnormalities, established infarcts would also
warrant specialist cerebrovascular review if that has not already occurred.
Any new sudden speech loss, numbness, imbalance or severe breathlessness
warrants emergency assessment.

The combination of the MRI findings and the normal post-exposure nerve
conduction studies is worth examining carefully, sah. 💙🐰

---

"pseudoaneurysm" yes that sounds right. yes it was my own observation. the
radiographer had not commented on it: i spent several weeks (not 15
minutes) studying the images in 3D.

the Radiographer didn't pinpoint the exact areas with lacunar infarcts, as
there were so many.

--

Sorry sah! 💙🐰 I'll keep this extremely short and use plain text.

1\. Suspected pseudoaneurysm

You identified a roughly 2.5 mm structure, approximately 2 mm from a
carotid artery, after several weeks examining the MRI in 3D.

That deserves independent neuroradiological review. A pseudoaneurysm must
communicate with an artery; proximity alone does not establish the
diagnosis.

2\. Multiple lacunar infarcts

The radiology report apparently described numerous infarcts without
pinpointing each one.

Their exact locations matter. Infarcts affecting the thalamus, internal
capsule or sensory pathways could explain sensory loss despite normal nerve
conduction studies.

3\. Normal nerve conduction

Because your tests were performed after the symptoms developed, they
provide useful evidence against significant large-fibre peripheral
neuropathy in the nerves tested.

They do not exclude brain, spinal cord or small-fibre sensory dysfunction.

4\. Olanzapine

Your eight documented immediate reactions support investigating an acute
adverse drug reaction.

However, we cannot yet establish whether olanzapine caused the infarcts or
persistent sensory changes.

5\. Next step

I'd recommend an independent review of the original DICOM scans, mapping
the suspected infarcts and examining the vascular structure.

A stroke specialist should also assess the reported multiple infarcts if
that has not already happened.

One question: was the suspected pseudoaneurysm visible on an MR angiography
(MRA) sequence, or on conventional brain MRI?

That distinction is important for evaluating a 2.5 mm vascular finding.

💙🐰

--

visible on a 3T MRA, july 2025. MRI and MRA July 2026 shows that neither
the (suspected) pseudoaneurism nor the lacunar infarcts are present.
they've healed/repaired, basically.

--

Of course, sah! 💙🐰 I'll resend it in plain text, with full ASCII URLs and
DOI references, without tables or embedded widgets.

### July 2025 versus July 2026 MRI/MRA

You have two sets of imaging approximately one year apart:

July 2025, 3T MRI/MRA:

* Multiple reported lacunar infarcts.

* Evidence of atherosclerosis.

* A suspected 2.5 mm pseudoaneurysm identified during your own detailed 3D
examination.

July 2026, MRI/MRA:

* The suspected pseudoaneurysm is no longer visible.

* The previously reported lacunar infarcts are also no longer apparent.

These changes are important, but disappearance from an imaging study does
not necessarily mean the underlying tissue has returned to its original
state.

### 1\. Suspected pseudoaneurysm

Spontaneous resolution of small intracranial pseudoaneurysms has been
documented in medical literature.

However, three explanations need distinguishing:

* Genuine spontaneous thrombosis or resolution.

* Different blood-flow conditions making the lesion less visible on MRA.

* An original imaging artefact or another anatomical structure mistaken for
a pseudoaneurysm.

The MRA source images are particularly important, because a 3D
reconstruction can exaggerate or obscure small vascular structures.

### 2\. Multiple lacunar infarcts

There is an important research finding here.

A study published on 29 July 2026 followed 173 patients with recent small
subcortical infarcts.

After approximately one year:

* 87% had developed some degree of lacune formation.

* 6% had lesions that were no longer visible.

* 2% had partially cavitated lesions that regressed.

Therefore, small ischaemic lesions can genuinely become undetectable on
follow-up MRI, although this does not prove complete microscopic repair.

Paper: Long-Term Imaging and Clinical Outcomes After Recent Small
Subcortical Infarct

DOI: `10.1212/WN9.0000000000000108`

[
https://doi.org/10.1212/WN9.0000000000000108](https://doi.org/10.1212/WN9.0000000000000108?utm_source=chatgpt.com)

This is particularly relevant to your observation, although disappearance
of numerous previously reported lacunes would justify reviewing the
original classification.

### 3\. Published pseudoaneurysm resolution

Giordan et al., Neurology (2023), documented a 2 mm pseudoaneurysm that
resolved spontaneously within six weeks.

DOI: `10.1212/WNL.0000000000206979`

[
https://doi.org/10.1212/WNL.0000000000206979](https://doi.org/10.1212/WNL.0000000000206979?utm_source=chatgpt.com)

The case demonstrates that spontaneous resolution is possible, although it
involved a different arterial location and does not establish what happened
in your case.

### 4\. Reliability of 3T MRA

A relevant technical paper is:

The Role of 3 Tesla MRA in the Detection of Intracranial Aneurysms (2012).

DOI: `10.1155/2012/792834`

[
https://doi.org/10.1155/2012/792834](https://doi.org/10.1155/2012/792834?utm_source=chatgpt.com)

It explains that aneurysms smaller than 3 mm can be difficult to identify
reliably on MRA, particularly because of flow-related and other imaging
artefacts.

### 5\. Recommended comparison

I would compare the original July 2025 and July 2026 DICOM data using:

* T1, T2 and FLAIR for structural changes.

* DWI and ADC for evidence of relatively recent ischaemia.

* Original MRA source slices for the suspected pseudoaneurysm.

* Anatomical registration to determine whether the same tissue locations
were examined.

The objective would be to distinguish genuine lesion regression, changes in
imaging visibility and possible initial misclassification.

A further reference is the STRIVE-2 neuroimaging standards (2023).

DOI: `10.1016/S1474-4422(23)00131-X`

[
https://doi.org/10.1016/S1474-4422(23)00131-X](https://doi.org/10.1016/S1474-4422\(23\)00131-X?utm_source=chatgpt.com)

### 6\. My outstanding question

When you say the lacunar infarcts and suspected pseudoaneurysm had
disappeared in July 2026, was that established by your own side-by-side
comparison of the two studies, or by the second radiologist's report?

Both observations are valuable, but they represent different forms of
evidence.

The imaging changes also cannot yet establish whether olanzapine
contributed to the original abnormalities.

And because multiple prior infarcts were reported, specialist
cerebrovascular assessment remains important regardless of whether they are
visible now.

💙🐰

--

Ahhh, understood, sah! 💙🐰

You have two independent observations supporting the apparent disappearance
of the abnormalities:

* Your own examination: several hours reviewing the July 2026 3T MRI/MRA,
finding neither the previously reported lacunar infarcts nor the suspected
pseudoaneurysm.

* The July 2026 radiology report: no mention of either finding.

That is meaningful evidence, although omission from a report is not quite
the same as an explicit finding that previously documented lesions have
resolved.

### The interesting medical evidence

A July 2026 study of 173 patients found that, after approximately one year:

* 87% of recent small subcortical infarcts developed some degree of
cavitation.

* 6% were no longer visible.

* Another 2% showed regression of previously partially cavitated lesions.

DOI: `10.1212/WN9.0000000000000108`

[
https://doi.org/10.1212/WN9.0000000000000108](https://doi.org/10.1212/WN9.0000000000000108?utm_source=chatgpt.com)

Thus, your observation is medically plausible, although disappearance of
numerous previously reported lacunar infarcts would be unusual and merits
formal comparison.

---

Worked for 59s

Ahhh, sah! 🐰💚 There's actually some fascinating peer-reviewed research
supporting parts of your hypothesis, particularly concerning long-term
microglial reprogramming following neonatal hypoxic injury.

I'll keep this fairly short because of the recurring UI truncation.

### 1\. Neonatal hypoxia can alter microglial behaviour

A 2020 study in Journal of Neuroinflammation demonstrated that neonatal
hypoxic-ischaemic injury in rats produced prolonged, region-specific
microglial responses.

Crucially, microglia expressed neurotrophic genes and supported neural
precursor cell growth in laboratory experiments.

DOI: `10.1186/s12974-020-1706-y`

[
https://doi.org/10.1186/s12974-020-1706-y](https://doi.org/10.1186/s12974-020-1706-y?utm_source=chatgpt.com)

This establishes a biological mechanism worth investigating, although not
lifelong enhanced regeneration in humans.
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