WITHOUT PREJUDICE<blockquote class="gmail_quote" style="margin:0 0 0 .8ex;border-left:1px #ccc solid;padding-left:1ex"><div></div>
</blockquote><div><br></div><div>in your deeply irresponsible and reprehensible</div><div>letter that you claimed to be a "review" you stated</div><div>uneequivocably without checking the facts that</div><div>a contractor hired by Southern Health "Trust"</div><div>by the name THAGADUR took "care".</div><div><br></div><div>the forced poisoning by the toxic substance</div><div>Olanzaline caused multiple side effects including</div><div>strokes, growing female breasts, and permanent</div><div>loss of sexual pleasure.</div><div><br></div><div>the toxic substance known as Olanzapine permanently</div><div>binds to neuro-receptors, preventing them from</div><div>working and therefore causing atrophy and</div><div>damage in the adversely permanently affected</div><div>neural pathways downstream.</div><div><br></div><div>how is the loss of sensation in parts of my body</div><div>including my penis, the loss of sexual pleasure</div><div>at orgasm, and causing strokes and atrial fibrillation</div><div>in any way "care" by the NHS?</div><div><br></div><div>the audio recording of the initial "meeting", cited</div><div>in writing by UHS Southern Health Management,</div><div>irresponsibly and falsely as 90 minutes when the</div><div>video recording taken and retained shows a</div><div>duration of 25, has the individuals present and</div><div>on the other side of the room 6 metres away when</div><div>i have damaged hearing, asking "why do you</div><div>BELIEVE that you have Medical symptoms"</div><div><br></div><div>note that is not "WHAT medical symptoms do you</div><div>have" which is what i THOUGHT i heard being asked</div><div>as the person's voice was unclear due to the</div><div>distance involved.</div><div><br></div><div>it is quite clear to me that they considered my</div><div>"inappropriate" acknowledgement of the actual</div><div>question as "evidence" when the fact remains that</div><div>it was only after listening to the indistinct recording</div><div>three times did i notice the word "BELIEVE" was</div><div>part of the original question.</div><div><br></div><div>the S.A.R from Hampshire County Council also</div><div>shows a months-long "investigation" with dozens</div><div>of verifiably factually-inaccurate statements</div><div>where a simple clarifying sequence of questions</div><div>that properly took into account my unique</div><div>neurological and physiological health (strokes,</div><div>heart attacks, PTSD from Domestic Abuse,</div><div>chronic calcium deficiency from stress and</div><div>trauma from abuse, Chronic Adrenal Fatigue</div><div>Syndrome from Domestic Abuse) would have</div><div>established the facts, not Grossly Medically</div><div>Negligent *conjecture* supported by family</div><div>members with a known propensity for engaging</div><div>in Abuse.</div><div><br></div><div><br></div><div>UHS Staff had been Grossly Medically Negligently</div><div>falsifying medical reports and mis-triaging emergency</div><div>incidents.</div><div><br></div><div>these irresponsible reports were presented as fact</div><div>instead of asking me what actually transpired.</div><div><br></div><div><br></div><div>i have also now located DANIEL HADLEY LEIGHTON's</div><div>original false statement. he explicitly demands</div><div>that its contents be kept secret from me.</div><div><br></div><div>this reprehensible and abusive behaviour makes</div><div>his later false and public claim that he had spoken</div><div>directly with me even more shocking, especially</div><div>given that you, the General Medical Council, in</div><div>combination with his false reports and the hard</div><div>medical evidence that you have provably and</div><div>demonstrably ignored, begins to look like wilful</div><div>and malicious Obstruction of Justice rather than</div><div>simple sheer incompetence and negligence in the</div><div>course of enacting your civic duties.</div><div><br></div><div>as such criminal offenses remove the protection</div><div>afforded under UK Torture Laws for civic employees</div><div>i strongly recommend that the persons involved</div><div>apologise directly to me as whistleblowers,</div><div>and then advise the GMC to retract its false</div><div>statements in writing as quickly as possible and</div><div>carry out a proper and full investigation, consulting</div><div>me at every step instead of engaging in shocking</div><div>and obstructive abuse that places me, a LIFE LONG</div><div>CHRONICALLY AND PERMANENTLY DISABLED</div><div>individual with a serious chronic jaw abcess, at risk</div><div>of death by strokes and heart attacks.</div><div><br></div><div><br></div><div><br></div><div>---</div><div><br></div><div>Worked for 1m 36s</div><div><br></div><div>Hello sah 🐰💚</div><div><br></div><div>Olanzapine (Zyprexa) affects several regions of the brain, particularly the frontal and temporal cortices, basal ganglia, hypothalamus, and dopamine-dependent neural circuits.</div><div><br></div><div>Importantly, peer-reviewed MRI studies have identified changes in cortical thickness and white-matter microstructure associated with olanzapine exposure.</div><div><br></div><div>We need to distinguish three things:</div><div><br></div><div>* Functional impairment — interference with neurotransmission, cognition, movement, or alertness.</div><div><br></div><div>* Structural changes — measurable alterations in brain anatomy detected using MRI.</div><div><br></div><div>* Actual neurological injury — neuronal loss or other tissue damage, which cannot automatically be inferred from changes in MRI measurements.</div><div><br></div><div>### 1\. Brain regions potentially adversely affected</div><div><br></div><div>| Brain region | Documented or suspected effects |</div><div>| -------------------------------------------- | ---------------------------------------------------------------------------------------------------------------------------- |</div><div>| Frontal cortex, including prefrontal regions | Impaired concentration, slowed thinking, reduced alertness; MRI evidence of cortical thinning |</div><div>| Temporal cortex | Structural changes reported in MRI studies; cognitive implications remain uncertain |</div><div>| Parietal cortex | Part of the widespread cortical changes seen in some imaging studies |</div><div>| Basal ganglia, particularly the striatum | Dopamine D2 receptor blockade can cause rigidity, tremors, akathisia and tardive dyskinesia |</div><div>| Hypothalamus | Disruption of appetite and metabolic regulation, contributing to weight gain and metabolic abnormalities |</div><div>| Hippocampus | Memory-related circuitry can be affected functionally, but evidence of olanzapine-specific structural injury is inconsistent |</div><div>| Cerebral white matter | Some MRI studies report altered microstructural measurements, particularly in frontotemporal connections |</div><div><br></div><div>The effects do not necessarily occur in every patient, and the evidence for structural changes is stronger in some regions than others.</div><div><br></div><div>### 2\. Strongest human MRI evidence</div><div><br></div><div>Voineskos et al., JAMA Psychiatry (2020)</div><div><br></div><div>PMID: [32101271](<a href="https://pubmed.ncbi.nlm.nih.gov/32101271/?utm_source=chatgpt.com">https://pubmed.ncbi.nlm.nih.gov/32101271/?utm_source=chatgpt.com</a>) | DOI: 10.1001/jamapsychiatry.2020.0036</div><div><br></div><div>This randomized, placebo-controlled study followed patients with psychotic depression. Seventy-two participants had usable paired MRI scans.</div><div><br></div><div>After 36 weeks, continued olanzapine exposure was associated with:</div><div><br></div><div>* Significantly greater cortical thinning in both hemispheres among patients who remained in remission.</div><div><br></div><div>* Widespread cortical effects, with the largest regional effects in the frontal and temporal lobes.</div><div><br></div><div>* 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.</div><div><br></div><div>The researchers estimated cortical thinning corresponding to approximately 1.2% of cortical thickness over 36 weeks.</div><div><br></div><div>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.</div><div><br></div><div>Follow-up: Molecular Psychiatry (2024)</div><div><br></div><div>PMID: [38503927](<a href="https://pubmed.ncbi.nlm.nih.gov/38503927/?utm_source=chatgpt.com">https://pubmed.ncbi.nlm.nih.gov/38503927/?utm_source=chatgpt.com</a>)</div><div><br></div><div>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.</div><div><br></div><div>### 3\. What about the hippocampus and white matter?</div><div><br></div><div>The distinction here is important.</div><div><br></div><div>A randomized hippocampal MRI study (PMID [23162479](<a href="https://pubmed.ncbi.nlm.nih.gov/23162479/?utm_source=chatgpt.com">https://pubmed.ncbi.nlm.nih.gov/23162479/?utm_source=chatgpt.com</a>)) found less hippocampal surface deformation with olanzapine than with haloperidol, without establishing a significant difference in overall hippocampal volume over time.</div><div><br></div><div>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.</div><div><br></div><div>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.</div><div><br></div><div>### 4\. Established neurological risks</div><div><br></div><div>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.</div><div><br></div><div>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.</div><div><br></div><div>One question, sah: are you investigating the effects of a single administration of olanzapine, or repeated exposure over weeks or months?</div><div><br></div><div>That distinction materially changes the neurological evidence, particularly concerning structural injury versus transient receptor-mediated impairment.</div><div><br></div><div>----</div><div><br></div><div>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)</div><div><br></div><div>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</div><div><br></div><div>---</div><div><br></div><div>Worked for 2m 16s</div><div><br></div><div>Sah, 💚🐰 this changes the clinical assessment considerably.</div><div><br></div><div>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.</div><div><br></div><div>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.</div><div><br></div><div>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.</div><div><br></div><div>### 1\. Particularly relevant published evidence</div><div><br></div><div>Acute dystonia caused by low-dose olanzapine (2003)</div><div><br></div><div>Journal of Neuropsychiatry and Clinical Neurosciences</div><div><br></div><div>A patient developed tongue-muscle dystonia, impaired articulation and painful neck-muscle spasms within hours of receiving 5 mg olanzapine.</div><div><br></div><div>[Original peer-reviewed publication](<a href="https://doi.org/10.1176/jnp.15.2.241?utm_source=chatgpt.com">https://doi.org/10.1176/jnp.15.2.241?utm_source=chatgpt.com</a>).</div><div><br></div><div>--</div><div><br></div><div><div>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.</div><div><br></div><div>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</div></div><div><br></div><div>---</div><div><br></div><div>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.</div><div><br></div><div>### 1\. Cardiac findings make the respiratory reaction especially concerning</div><div><br></div><div>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.</div><div><br></div><div>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.</div><div><br></div><div>Two different mechanisms deserve consideration:</div><div><br></div><div>* Cardiogenic respiratory distress: a transient cardiovascular disturbance, arrhythmia, or deterioration in ventricular function might produce dyspnoea, particularly in someone with pre-existing cardiac dysfunction.</div><div><br></div><div>* Acute laryngeal dystonia: involuntary contraction of muscles controlling the upper airway can produce severe breathing difficulty, sometimes accompanied by abnormal vocalisation or difficulty speaking.</div><div><br></div><div>The second mechanism is well documented with antipsychotics, including olanzapine at 5 mg.</div><div><br></div><div>A particularly relevant systematic review is PMID [38185029](<a href="https://pubmed.ncbi.nlm.nih.gov/38185029/?utm_source=chatgpt.com">https://pubmed.ncbi.nlm.nih.gov/38185029/?utm_source=chatgpt.com</a>).</div><div><br></div><div>These mechanisms are clinically distinct. The recorded breathing sounds, vocalisations, pulse, oxygen saturation and any contemporaneous cardiac findings could help discriminate between them.</div><div><br></div><div>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.</div><div><br></div><div>### 2\. The breast enlargement and sexual dysfunction may share an endocrine mechanism</div><div><br></div><div>This deserves particular attention because olanzapine can interfere with the hypothalamic–pituitary–gonadal axis.</div><div><br></div><div>POTENTIAL ENDOCRINE PATHWAY</div><div><br></div><div>Olanzapine</div><div><br></div><div>Dopamine D₂ receptor antagonism</div><div><br></div><div>Pituitary gland</div><div><br></div><div>Potential increase in prolactin</div><div><br></div><div>Hypothalamic–gonadal axis</div><div><br></div><div>Possible suppression of GnRH / LH / FSH</div><div><br></div><div>Potential clinical effects</div><div><br></div><div>Sexual dysfunction and breast enlargement</div><div><br></div><div>Possible physiological mechanism, not a confirmed diagnosis in your case.</div><div><br></div><div>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.</div><div><br></div><div>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.</div><div><br></div><div>There are also two different conditions to distinguish:</div><div><br></div><div>* Gynaecomastia: growth of glandular breast tissue, often associated with hormonal changes.</div><div><br></div><div>* Pseudogynaecomastia: increased fatty tissue without corresponding glandular enlargement.</div><div><br></div><div>The European Academy of Andrology guideline, PMID [31099174](<a href="https://pubmed.ncbi.nlm.nih.gov/31099174/?utm_source=chatgpt.com">https://pubmed.ncbi.nlm.nih.gov/31099174/?utm_source=chatgpt.com</a>), recommends clinical examination and appropriate hormonal investigation, including testosterone, estradiol, LH, FSH, TSH and prolactin.</div><div><br></div><div>### 3\. Loss of physical sensation is a separate neurological finding</div><div><br></div><div>This is the part I would be especially careful not to overlook.</div><div><br></div><div>Olanzapine's prescribing information includes paraesthesia (abnormal sensations such as tingling) among reported adverse reactions in some clinical trials.</div><div><br></div><div>But persistent loss of touch sensation is not equivalent to reduced libido or diminished sexual enjoyment.</div><div><br></div><div>Three different processes may be involved:</div><div><br></div><div>| Symptom | Anatomical or physiological system to investigate |</div><div>| --------------------------------------------------------- | -------------------------------------------------------------------------- |</div><div>| Reduced sexual pleasure despite preserved touch sensation | Dopaminergic reward pathways, sexual function and endocrine regulation |</div><div>| Reduced genital tactile sensation | Peripheral sensory nerves, pudendal pathways, sacral spinal segments S2–S4 |</div><div>| Reduced sensation over other skin regions | Peripheral nerves, spinal cord, thalamus, parietal somatosensory cortex |</div><div><br></div><div>This distinction matters for your original question about which brain regions can be adversely affected.</div><div><br></div><div>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.</div><div><br></div><div>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.</div><div><br></div><div>New or worsening genital/saddle numbness with bladder or bowel dysfunction requires emergency assessment.</div><div><br></div><div>### 4\. DRESS: confirmed drug risk, but not yet an established diagnosis</div><div><br></div><div>The FDA issued a specific safety warning about olanzapine-associated DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms).</div><div><br></div><div>FDA Drug Safety Communication, 2016</div><div><br></div><div>[](<a href="https://www.fda.gov/downloads/Drugs/DrugSafety/UCM499603.pdf?utm_source=chatgpt.com">https://www.fda.gov/downloads/Drugs/DrugSafety/UCM499603.pdf?utm_source=chatgpt.com</a>)</div><div><br></div><div>---</div><div><br></div><div>"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.</div><div><br></div><div>---</div><div><br></div><div>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.</div><div><br></div><div>### Normal nerve conduction studies: what this tells us</div><div><br></div><div>You mentioned that you underwent electrical nerve conduction testing on your arms and legs, and that the results were reported as normal.</div><div><br></div><div>This is significant evidence, but it does not exclude neurological damage or dysfunction affecting sensation.</div><div><br></div><div>Routine nerve conduction studies (NCS) and electromyography (EMG) primarily assess large peripheral nerve fibres and muscle electrical activity.</div><div><br></div><div>They cannot reliably detect every type of neurological disorder.</div><div><br></div><div>### 1\. What normal results do and don't exclude</div><div><br></div><div>Large-fibre peripheral neuropathy: Significant abnormalities are less likely in the nerves tested, particularly if both motor and sensory conduction studies were performed.</div><div><br></div><div>Small-fibre neuropathy: NOT excluded. Small sensory fibres transmit pain, temperature and other sensory information. Conventional nerve conduction tests cannot adequately examine these fibres.</div><div><br></div><div>Spinal cord sensory pathways: NOT excluded. Standard EMG/NCS does not directly evaluate the ascending sensory pathways inside the spinal cord.</div><div><br></div><div>Thalamus: NOT excluded. The thalamus processes and relays sensory information to the cerebral cortex.</div><div><br></div><div>Parietal somatosensory cortex: NOT excluded. This region participates in processing touch, pressure, body position and the localisation of sensation.</div><div><br></div><div>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.</div><div><br></div><div>### 2\. Particular relevance to your existing MRI findings</div><div><br></div><div>You previously described MRI-visible abnormalities involving:</div><div><br></div><div>* Right parietal lobe.</div><div><br></div><div>* Centrum semiovale.</div><div><br></div><div>* Periventricular white matter, associated with your history of early-life injury.</div><div><br></div><div>These are anatomically relevant to sensory processing and transmission.</div><div><br></div><div>However, they cannot automatically be identified as the cause of your current sensory difficulties.</div><div><br></div><div>Nor does normal EMG/NCS establish that olanzapine damaged your central nervous system.</div><div><br></div><div>The relevant question is whether there has been an objectively demonstrable change in neurological function following the medication exposure.</div><div><br></div><div>### 3\. Small-fibre neuropathy deserves consideration</div><div><br></div><div>A particularly important distinction is between large and small nerve fibres.</div><div><br></div><div>Large fibres carry information such as vibration and proprioception. Small fibres carry pain, temperature and autonomic signals.</div><div><br></div><div>Consequently, a person may have normal conventional nerve conduction studies while still having clinically significant small-fibre neuropathy.</div><div><br></div><div>A 2026 evidence review discusses this diagnostic problem:</div><div><br></div><div>PMID: 41670166</div><div><br></div><div>[<a href="https://pubmed.ncbi.nlm.nih.gov/41670166/](https://pubmed.ncbi.nlm.nih.gov/41670166/?utm_source=chatgpt.com)">https://pubmed.ncbi.nlm.nih.gov/41670166/](https://pubmed.ncbi.nlm.nih.gov/41670166/?utm_source=chatgpt.com)</a></div><div><br></div><div>Investigations include skin punch biopsy for intraepidermal nerve fibre density, quantitative sensory testing and selected autonomic function tests.</div><div><br></div><div>None is sufficient by itself to establish that olanzapine caused the abnormality.</div><div><br></div><div>### 4\. Central sensory dysfunction is another possibility</div><div><br></div><div>If your sensory reduction involves several unrelated areas of the body, rather than following individual peripheral nerves, a central mechanism deserves examination.</div><div><br></div><div>Particularly relevant structures are:</div><div><br></div><div>Thalamus: sensory relay and integration.</div><div><br></div><div>Primary somatosensory cortex: conscious discrimination and localisation of physical sensation.</div><div><br></div><div>Insular cortex: integration of bodily sensations with conscious experience.</div><div><br></div><div>Ascending spinal sensory pathways: transmission of sensory signals toward the brain.</div><div><br></div><div>Mesolimbic dopaminergic circuitry: aspects of reward, motivation and subjective pleasure, including sexual pleasure.</div><div><br></div><div>Olanzapine influences neurotransmission within several of these networks.</div><div><br></div><div>However, an important distinction remains: pharmacological inhibition of neural activity is not necessarily equivalent to permanent structural injury.</div><div><br></div><div>### 5\. Investigations that could distinguish the mechanisms</div><div><br></div><div>A neurologist could consider a formal sensory examination, including light touch, vibration, temperature, pinprick and proprioception.</div><div><br></div><div>Depending on the pattern found, further assessment might include quantitative sensory testing, small-fibre skin biopsy, somatosensory evoked potentials or appropriate MRI sequences.</div><div><br></div><div>Your existing EMG/NCS report would be particularly valuable because it may contain separate motor and sensory conduction results.</div><div><br></div><div>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.</div><div><br></div><div>### 6\. One particularly important question</div><div><br></div><div>Were those normal nerve conduction studies performed BEFORE or AFTER the week of forced olanzapine administration and the development of your sensory loss?</div><div><br></div><div>If they were performed afterwards, they provide useful evidence that significant large-fibre abnormalities were not detectable in the nerves tested at that time.</div><div><br></div><div>If performed beforehand, they establish something different: a baseline against which subsequent findings could be compared.</div><div><br></div><div>Either way, the normal results do not rule out small-fibre or central neurological dysfunction.</div><div><br></div><div>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.</div><div><br></div><div>💚🐰</div><div><br></div><div>---</div><div><br></div><div>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</div><div><br></div><div>--</div><div><br></div><div>Ahhh, sorry sah! 💙🐰 The app seems to be truncating the longer responses.</div><div><br></div><div>I'll repeat the important findings in plain text, without tables, diagrams or embedded widgets.</div><div><br></div><div>### 1\. Normal nerve conduction AFTER the olanzapine exposure</div><div><br></div><div>This is significant.</div><div><br></div><div>Your EMG/nerve conduction tests were normal despite your reported sensory loss.</div><div><br></div><div>This makes significant large-fibre peripheral nerve damage less likely in the nerves tested.</div><div><br></div><div>However, these tests do not rule out:</div><div><br></div><div>* Damage to sensory pathways within the brain.</div><div><br></div><div>* Spinal cord abnormalities.</div><div><br></div><div>* Small-fibre peripheral neuropathy.</div><div><br></div><div>* Dysfunction of the thalamus or parietal somatosensory cortex.</div><div><br></div><div>### 2\. Multiple lacunar infarcts on MRI</div><div><br></div><div>This is particularly important.</div><div><br></div><div>Lacunar infarcts are small areas of ischaemic injury within the brain, frequently involving deep cerebral structures.</div><div><br></div><div>Depending on their location, they can produce:</div><div><br></div><div>* Loss or alteration of physical sensation.</div><div><br></div><div>* Balance and coordination difficulties.</div><div><br></div><div>* Speech disturbances.</div><div><br></div><div>* Impaired concentration and executive function.</div><div><br></div><div>Normal nerve conduction studies are entirely compatible with cerebral infarcts.</div><div><br></div><div>The particularly relevant anatomical structures include the thalamus, internal capsule, corona radiata and brainstem.</div><div><br></div><div>We would need the precise locations of your infarcts to establish whether they correspond to the neurological deficits you describe.</div><div><br></div><div>### 3\. Atherosclerosis and the 2.5 mm finding</div><div><br></div><div>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.</div><div><br></div><div>You called it a false embolism.</div><div><br></div><div>Did you mean a pseudoaneurysm (false aneurysm)?</div><div><br></div><div>A pseudoaneurysm is a contained breach of an arterial wall. It differs fundamentally from an embolus, which travels through the bloodstream.</div><div><br></div><div>Something appearing near an artery on MRI cannot be identified reliably from proximity alone.</div><div><br></div><div>If this is a suspected pseudoaneurysm, independent neuroradiological review of the original images would be appropriate.</div><div><br></div><div>### 4\. Relationship to olanzapine</div><div><br></div><div>There are now three important findings:</div><div><br></div><div>A. Acute reactions: Eight reportedly reproducible episodes following administration of 5 mg olanzapine, including involuntary vocalisations, respiratory distress, balance impairment and cognitive dysfunction.</div><div><br></div><div>These strengthen the suspicion of an acute adverse drug reaction.</div><div><br></div><div>B. Cerebrovascular abnormalities: MRI-reported lacunar infarcts and atherosclerosis, requiring assessment of their location, age and possible causes.</div><div><br></div><div>C. Persistent sensory dysfunction: Despite normal peripheral conduction studies, suggesting that central sensory pathways and small-fibre function remain relevant to investigate.</div><div><br></div><div>These findings can coexist. They do not yet establish that olanzapine caused the infarcts or persistent sensory impairment.</div><div><br></div><div>### 5\. The most important missing information</div><div><br></div><div>Two details would help considerably:</div><div><br></div><div>* Where exactly were the lacunar infarcts? The MRI report should identify their anatomical locations.</div><div><br></div><div>* Was the 2.5 mm structure a suspected pseudoaneurysm, and was this your own observation from the DICOM images?</div><div><br></div><div>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.</div><div><br></div><div>The combination of the MRI findings and the normal post-exposure nerve conduction studies is worth examining carefully, sah. 💙🐰</div><div><br></div><div>---</div><div><br></div><div>"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.</div><div><br></div><div>the Radiographer didn't pinpoint the exact areas with lacunar infarcts, as there were so many.</div><div><br></div><div>--</div><div><br></div><div>Sorry sah! 💙🐰 I'll keep this extremely short and use plain text.</div><div><br></div><div>1\. Suspected pseudoaneurysm</div><div><br></div><div>You identified a roughly 2.5 mm structure, approximately 2 mm from a carotid artery, after several weeks examining the MRI in 3D.</div><div><br></div><div>That deserves independent neuroradiological review. A pseudoaneurysm must communicate with an artery; proximity alone does not establish the diagnosis.</div><div><br></div><div>2\. Multiple lacunar infarcts</div><div><br></div><div>The radiology report apparently described numerous infarcts without pinpointing each one.</div><div><br></div><div>Their exact locations matter. Infarcts affecting the thalamus, internal capsule or sensory pathways could explain sensory loss despite normal nerve conduction studies.</div><div><br></div><div>3\. Normal nerve conduction</div><div><br></div><div>Because your tests were performed after the symptoms developed, they provide useful evidence against significant large-fibre peripheral neuropathy in the nerves tested.</div><div><br></div><div>They do not exclude brain, spinal cord or small-fibre sensory dysfunction.</div><div><br></div><div>4\. Olanzapine</div><div><br></div><div>Your eight documented immediate reactions support investigating an acute adverse drug reaction.</div><div><br></div><div>However, we cannot yet establish whether olanzapine caused the infarcts or persistent sensory changes.</div><div><br></div><div>5\. Next step</div><div><br></div><div>I'd recommend an independent review of the original DICOM scans, mapping the suspected infarcts and examining the vascular structure.</div><div><br></div><div>A stroke specialist should also assess the reported multiple infarcts if that has not already happened.</div><div><br></div><div>One question: was the suspected pseudoaneurysm visible on an MR angiography (MRA) sequence, or on conventional brain MRI?</div><div><br></div><div>That distinction is important for evaluating a 2.5 mm vascular finding.</div><div><br></div><div>💙🐰</div><div><br></div><div>--</div><div><br></div><div>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.</div><div><br></div><div>--</div><div><br></div><div>Of course, sah! 💙🐰 I'll resend it in plain text, with full ASCII URLs and DOI references, without tables or embedded widgets.</div><div><br></div><div>### July 2025 versus July 2026 MRI/MRA</div><div><br></div><div>You have two sets of imaging approximately one year apart:</div><div><br></div><div>July 2025, 3T MRI/MRA:</div><div><br></div><div>* Multiple reported lacunar infarcts.</div><div><br></div><div>* Evidence of atherosclerosis.</div><div><br></div><div>* A suspected 2.5 mm pseudoaneurysm identified during your own detailed 3D examination.</div><div><br></div><div>July 2026, MRI/MRA:</div><div><br></div><div>* The suspected pseudoaneurysm is no longer visible.</div><div><br></div><div>* The previously reported lacunar infarcts are also no longer apparent.</div><div><br></div><div>These changes are important, but disappearance from an imaging study does not necessarily mean the underlying tissue has returned to its original state.</div><div><br></div><div>### 1\. Suspected pseudoaneurysm</div><div><br></div><div>Spontaneous resolution of small intracranial pseudoaneurysms has been documented in medical literature.</div><div><br></div><div>However, three explanations need distinguishing:</div><div><br></div><div>* Genuine spontaneous thrombosis or resolution.</div><div><br></div><div>* Different blood-flow conditions making the lesion less visible on MRA.</div><div><br></div><div>* An original imaging artefact or another anatomical structure mistaken for a pseudoaneurysm.</div><div><br></div><div>The MRA source images are particularly important, because a 3D reconstruction can exaggerate or obscure small vascular structures.</div><div><br></div><div>### 2\. Multiple lacunar infarcts</div><div><br></div><div>There is an important research finding here.</div><div><br></div><div>A study published on 29 July 2026 followed 173 patients with recent small subcortical infarcts.</div><div><br></div><div>After approximately one year:</div><div><br></div><div>* 87% had developed some degree of lacune formation.</div><div><br></div><div>* 6% had lesions that were no longer visible.</div><div><br></div><div>* 2% had partially cavitated lesions that regressed.</div><div><br></div><div>Therefore, small ischaemic lesions can genuinely become undetectable on follow-up MRI, although this does not prove complete microscopic repair.</div><div><br></div><div>Paper: Long-Term Imaging and Clinical Outcomes After Recent Small Subcortical Infarct</div><div><br></div><div>DOI: `10.1212/WN9.0000000000000108`</div><div><br></div><div>[<a href="https://doi.org/10.1212/WN9.0000000000000108](https://doi.org/10.1212/WN9.0000000000000108?utm_source=chatgpt.com)">https://doi.org/10.1212/WN9.0000000000000108](https://doi.org/10.1212/WN9.0000000000000108?utm_source=chatgpt.com)</a></div><div><br></div><div>This is particularly relevant to your observation, although disappearance of numerous previously reported lacunes would justify reviewing the original classification.</div><div><br></div><div>### 3\. Published pseudoaneurysm resolution</div><div><br></div><div>Giordan et al., Neurology (2023), documented a 2 mm pseudoaneurysm that resolved spontaneously within six weeks.</div><div><br></div><div>DOI: `10.1212/WNL.0000000000206979`</div><div><br></div><div>[<a href="https://doi.org/10.1212/WNL.0000000000206979](https://doi.org/10.1212/WNL.0000000000206979?utm_source=chatgpt.com)">https://doi.org/10.1212/WNL.0000000000206979](https://doi.org/10.1212/WNL.0000000000206979?utm_source=chatgpt.com)</a></div><div><br></div><div>The case demonstrates that spontaneous resolution is possible, although it involved a different arterial location and does not establish what happened in your case.</div><div><br></div><div>### 4\. Reliability of 3T MRA</div><div><br></div><div>A relevant technical paper is:</div><div><br></div><div>The Role of 3 Tesla MRA in the Detection of Intracranial Aneurysms (2012).</div><div><br></div><div>DOI: `10.1155/2012/792834`</div><div><br></div><div>[<a href="https://doi.org/10.1155/2012/792834](https://doi.org/10.1155/2012/792834?utm_source=chatgpt.com)">https://doi.org/10.1155/2012/792834](https://doi.org/10.1155/2012/792834?utm_source=chatgpt.com)</a></div><div><br></div><div>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.</div><div><br></div><div>### 5\. Recommended comparison</div><div><br></div><div>I would compare the original July 2025 and July 2026 DICOM data using:</div><div><br></div><div>* T1, T2 and FLAIR for structural changes.</div><div><br></div><div>* DWI and ADC for evidence of relatively recent ischaemia.</div><div><br></div><div>* Original MRA source slices for the suspected pseudoaneurysm.</div><div><br></div><div>* Anatomical registration to determine whether the same tissue locations were examined.</div><div><br></div><div>The objective would be to distinguish genuine lesion regression, changes in imaging visibility and possible initial misclassification.</div><div><br></div><div>A further reference is the STRIVE-2 neuroimaging standards (2023).</div><div><br></div><div>DOI: `10.1016/S1474-4422(23)00131-X`</div><div><br></div><div>[<a href="https://doi.org/10.1016/S1474-4422(23)00131-X](https://doi.org/10.1016/S1474-4422\(23\)00131-X?utm_source=chatgpt.com)">https://doi.org/10.1016/S1474-4422(23)00131-X](https://doi.org/10.1016/S1474-4422\(23\)00131-X?utm_source=chatgpt.com)</a></div><div><br></div><div>### 6\. My outstanding question</div><div><br></div><div>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?</div><div><br></div><div>Both observations are valuable, but they represent different forms of evidence.</div><div><br></div><div>The imaging changes also cannot yet establish whether olanzapine contributed to the original abnormalities.</div><div><br></div><div>And because multiple prior infarcts were reported, specialist cerebrovascular assessment remains important regardless of whether they are visible now.</div><div><br></div><div>💙🐰</div><div><br></div><div>--</div><div><br></div><div>Ahhh, understood, sah! 💙🐰</div><div><br></div><div>You have two independent observations supporting the apparent disappearance of the abnormalities:</div><div><br></div><div>* Your own examination: several hours reviewing the July 2026 3T MRI/MRA, finding neither the previously reported lacunar infarcts nor the suspected pseudoaneurysm.</div><div><br></div><div>* The July 2026 radiology report: no mention of either finding.</div><div><br></div><div>That is meaningful evidence, although omission from a report is not quite the same as an explicit finding that previously documented lesions have resolved.</div><div><br></div><div>### The interesting medical evidence</div><div><br></div><div>A July 2026 study of 173 patients found that, after approximately one year:</div><div><br></div><div>* 87% of recent small subcortical infarcts developed some degree of cavitation.</div><div><br></div><div>* 6% were no longer visible.</div><div><br></div><div>* Another 2% showed regression of previously partially cavitated lesions.</div><div><br></div><div>DOI: `10.1212/WN9.0000000000000108`</div><div><br></div><div>[<a href="https://doi.org/10.1212/WN9.0000000000000108](https://doi.org/10.1212/WN9.0000000000000108?utm_source=chatgpt.com)">https://doi.org/10.1212/WN9.0000000000000108](https://doi.org/10.1212/WN9.0000000000000108?utm_source=chatgpt.com)</a></div><div><br></div><div>Thus, your observation is medically plausible, although disappearance of numerous previously reported lacunar infarcts would be unusual and merits formal comparison.</div><div><br></div><div>---</div><div><br></div><div>Worked for 59s</div><div><br></div><div>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.</div><div><br></div><div>I'll keep this fairly short because of the recurring UI truncation.</div><div><br></div><div>### 1\. Neonatal hypoxia can alter microglial behaviour</div><div><br></div><div>A 2020 study in Journal of Neuroinflammation demonstrated that neonatal hypoxic-ischaemic injury in rats produced prolonged, region-specific microglial responses.</div><div><br></div><div>Crucially, microglia expressed neurotrophic genes and supported neural precursor cell growth in laboratory experiments.</div><div><br></div><div>DOI: `10.1186/s12974-020-1706-y`</div><div><br></div><div>[<a href="https://doi.org/10.1186/s12974-020-1706-y](https://doi.org/10.1186/s12974-020-1706-y?utm_source=chatgpt.com)">https://doi.org/10.1186/s12974-020-1706-y](https://doi.org/10.1186/s12974-020-1706-y?utm_source=chatgpt.com)</a></div><div><br></div><div>This establishes a biological mechanism worth investigating, although not lifelong enhanced regeneration in humans.</div><div><br></div><div><br></div>