BREACH OF HUMAN RIGHTS BY LPFT AND INJURY CAUSED BY FREQUENT RT/PLANS FOR CARE OUT OF AREA AGAINST ELIZABETH’S WISHES AND THAT OF HER FAMILY.

I managed to get to speak to my daughter who was passed her mobile phone kept locked away in the office right now which according to LINCOLNSHIRE PARTNERSHIP TRUST IS IN LINE WITH HUMAN RIGHTS.

I was worried for her safety the other day having heard she was having an episode.

I am going to write all about the injury my daughter is suffering and the frequent episodes and constant rapid tranquilisations Castle Ward are giving on virtually a daily basis. I now want all the scans re-looked at as nothing can be relied upon under Lincolnshire who only have a 1.5 scanner. In my previous blogs I have included some interesting research papers on 1.5 MRI as opposed to Tesla 3. A Tesla 3 is why the private scans I had done revealed details not visible on a 1.5 scanner and I am warning everyone to check on which scanner their Trust has.

The restrictions are supposed to have ended on 5 February but continue with phone locked away and visits heavily restricted 2-1 supervised. Elizabeth said she misses not being able to listen to music on her phone. I am going to invoice LPFT for the contract as it is not being used. It was during my conversation with Elizabeth that she mentioned Castle Ward want to film her on the advice of the Neurologist when she has an episode. How can this be accurate and I want things accurate and to be 100% sure and the only way for this is for Elizabeth to be referred under S17 leave to Sheffield where they have a Tesla 3 scanner and a proper ward for neurology. This would need to be granted by Dr Waqqas khokhar as currently she has no leave entitlement whatsoever. Elizabeth said she did not want to be filmed by the MH team but did not mind being monitored by the Neurologist team in Sheffield provided she was given a takeaway. I said I am sure this could be arranged. Elizabeth would need to be closely monitored but this is essential. She said she would be happy to be monitored by experts in Sheffield . I am now extremely concerned that the MH team will try and send her to a supported living to avoid any pathological tests that need to be done because of the frequent fits. This must be determined first and foremost in a specialist hospital. Elizabeth has said on numerous occasions she does not wish to go into supported living which has been tried and totally failed before especially when she has an independent bungalow and even a two bed static caravan in the back garden. I am appalled and disgusted at what LPFT are doing when all along they should have taken a strong interest in her physical health and I am disclosing some interesting information below and the disturbing facts.

Subject: Neuroplasticity and Rapid Tranquillisation!

Neuroplasticity & Concomitant Drug ADRs:     

Here are some potential explanations for the psychomotor ‘episodes’ Elizabeth has been experiencing.   

The reason the episodes are getting more frequent is explained below.  The frequency of the PRN is so short that the previous dose has not fully metabolised before they give her another one. 

There is also a possibility that the depot anti-psychotic medication concomitantly administered with rapid tranquillisation is causing psychomotor dysfunction. 

Chronic treatment with antipsychotic medications like Clopixol has been associated with alterations in brain structure and neuroplasticity, including changes in grey matter volume, dendritic spine density, and synaptic connectivity.

Benzodiazepines have also been shown to influence synaptic plasticity, albeit through different mechanisms. 

The concomitant use of Clopixol and benzodiazepines may potentially interact to modulate neuroplasticity.

Chronic benzodiazepine use, such as repeated PRN rapid tranquillisation may be associated with alterations in brain structure and function. These changes may include reductions in grey matter volume, alterations in neurotransmitter systems, and neuroplastic changes.  Neuroplastic changes will show up on a 3 Tesla MRI scanner.  Presumably that is why certain people might not want such a scan done.  

Neuroplastic changes can be detected using a 3 Tesla magnetic resonance imaging (MRI) scanner. A 3 Tesla MRI scanner is a powerful imaging tool that provides high-resolution images of the brain and has become the standard in clinical and research settings for studying brain structure and function.

Neuroplasticity refers to the brain’s ability to reorganize and adapt in response to experiences, learning, and environmental stimuli. These changes can occur at various levels, including alterations in synaptic connectivity, changes in neuronal morphology, and modifications in functional connectivity between brain regions.

With advanced imaging techniques such as functional MRI (fMRI), diffusion tensor imaging (DTI), and structural MRI, researchers and clinicians can visualize and quantify neuroplastic changes in the brain.

Here are a few examples of how neuroplasticity can be observed using a 3 Tesla MRI scanner:

1.     Functional MRI (fMRI): fMRI measures changes in blood flow and oxygenation levels in the brain, which reflect neuronal activity. By analysing fMRI data, researchers can identify changes in brain activation patterns associated with learning, memory, and other cognitive processes, providing insights into neuroplasticity.

2.     Structural MRI: Structural MRI techniques can detect changes in brain structure, including alterations in grey matter volume, cortical thickness, and white matter integrity. These changes may result from neuroplastic processes such as dendritic growth, synaptogenesis, and myelination, which can be visualized and quantified using high-resolution structural MRI scans.

3.     Diffusion MRI (DTI): DTI measures the diffusion of water molecules in brain tissue and provides information about the microstructural organization of white matter pathways. By analysing DTI data, researchers can map changes in white matter integrity, such as alterations in fibre density, orientation, and connectivity, which are indicative of neuroplastic changes in the brain.

Overall, a 3 Tesla MRI scanner is capable of detecting and characterising neuroplastic changes in the brain, providing valuable insights into the mechanisms underlying learning, memory, recovery from injury, and adaptation to environmental stimuli. These imaging techniques play a crucial role in advancing our understanding of neuroplasticity and its implications for brain health and function.

Repeated rapid tranquilization with benzodiazepines can potentially lead to psychomotor dysfunction, although the likelihood and severity of this side effect may vary depending on factors such as the specific benzodiazepine used, the dosage, frequency of administration, individual susceptibility, and concurrent use of other medications.

Psychomotor dysfunction refers to impairments in motor coordination, reaction time, and cognitive function, which can manifest as symptoms such as drowsiness, dizziness, confusion, ataxia (loss of coordination), and impaired judgment.  (this is what they mean by episodes) Benzodiazepines exert their effects on the central nervous system by enhancing the activity of the neurotransmitter gamma-aminobutyric acid (GABA), which can lead to sedation and relaxation.

During rapid tranquilisation, benzodiazepines are often administered to quickly alleviate acute agitation, aggression, or psychosis in emergency situations. While benzodiazepines can effectively reduce agitation and aggression, they can also cause sedation and other central nervous system depressant effects, particularly at higher doses or with rapid administration.

Repeated administration of benzodiazepines for rapid tranquilization may increase the risk of cumulative sedation and psychomotor dysfunction, especially if doses are given close together or if there is insufficient time for the drug to be metabolized and eliminated from the body between administrations. Additionally, certain factors such as age, medical conditions, and concurrent use of other medications may increase the susceptibility to benzodiazepine-induced psychomotor dysfunction.

Metabolism of benzodiazepines primarily occurs in the liver, where they undergo hepatic biotransformation mediated by various cytochrome P450 (CYP) enzymes, particularly CYP3A4, CYP2C19, and CYP2D6. Endocrine dysfunctions can affect the activity of these metabolic enzymes through various mechanisms, potentially leading to alterations in benzodiazepine metabolism.

It is essential for healthcare providers to carefully monitor patients who receive repeated rapid tranquilization with benzodiazepines for signs of psychomotor dysfunction and to adjust treatment accordingly to minimize the risk of adverse effects. Alternative strategies for managing agitation and aggression should also be considered, and the use of benzodiazepines should be limited to situations where the benefits outweigh the potential risks.

There is evidence to suggest that chronic benzodiazepine use may be associated with alterations in synaptic plasticity, which refers to the ability of synapses to strengthen or weaken over time in response to activity. Chronic benzodiazepine use has been shown to lead to changes in neurotransmitter systems, including alterations in GABA receptor expression and function, as well as changes in the density and morphology of dendritic spines, the small protrusions on neurons where synapses form.

These changes in synaptic plasticity may have implications for neuronal connectivity and brain function, although the extent to which benzodiazepines directly disrupt synaptic connectivity is not fully understood. Additionally, the clinical significance of these changes in synaptic plasticity in relation to the therapeutic effects and potential side effects of benzodiazepine use requires further investigation.

The increase in the frequency of the episodes you describe could indicate a condition known as dopamine supersensitivity psychosis.  This is seen both with typical and atypical antipsychotics.  The prolonged use of anti-psychotics that are not working due to her inability to metabolise anti-psychotics gives rise for concern.  Has it not crossed anyone’s mind in that ‘treatment team’ that in spite of being on Clopixol for years she has not shown any sign of it being efficacious.    

Since Elizabeth has never fully responded to the anti-psychotic medication they give her and they use PRN benzodiazepines for rapid tranquillisation far too frequently it is not surprising that she is having psychomotor problems.  In effect this is another form of TD.  If she is supersensitive then any dopamine antagonist could very well be causing this ADR.  

A high resolution scan will indicate inflammation in the meso-limbic pathway affecting the dopamine receptors.  The 1.5 Tesla scanner does not have sufficient resolution to do this. Inflammation can cause psychomotor problems as well as psychotic symptoms.  Perhaps if they took the time to look for this specific adverse reaction they might not conclude the rather odd idea that the scan is normal.    

By the way, the information I have on this is from The British Journal of Psychopharmacology just in case LPFT decide to dismiss this also.  

Why 3T is necessary for detecting lesions

· ■ In more than 500 follow-up images, only four of 1996 new or enlarged multiple sclerosis lesions would have been missed with 3.0-T MRI without the administration of contrast material.

· ■ With 3.0-T MRI, the assessment of interval progression did not differ between contrast-enhanced and nonenhanced images.

Introduction

Inflammatory lesions in multiple sclerosis (MS) are detected as focal areas of high signal intensity on T2-weighted MR images. By depicting newly occurring lesions, MRI reveals subclinical disease activity. Therefore, regular follow-up MRI is considered a mainstay of clinical care for patients with MS or clinically isolated syndromes.

Earlier studies have reported that the administration of contrast material is necessary to maximize sensitivity for detecting new lesions. However, these results date back more than 2 decades and were based on two-dimensional images obtained with 4–5-mm-thick sections at magnetic field strengths of 1.5 T and lower.

MRI units with higher field strengths have become widely available, especially for brain imaging. In addition, three-dimensional isotropic MRI sequences were introduced and were shown to outperform conventional two-dimensional sequences in lesion depiction; they are therefore part of recommended MRI standards in MS . Furthermore, the double inversion-recovery (DIR) sequence was introduced. Although this sequence is best known for its ability to depict cortical lesions, it is also useful for depicting white matter lesions Recently, longitudinal subtraction techniques have been developed that show new or enlarged lesions as bright spots while pre-existing lesions and normal-appearing brain parenchyma are canceled out.* Such techniques substantially improve the sensitivity in the detection of new or enlarged lesions in MS at follow-up imaging.

We hypothesized that the use of contrast material does not improve sensitivity in the detection of new or enlarged lesions at follow-up MRI when modern three-dimensional sequences performed at a field strength of 3.0 T are used together with longitudinal subtraction maps. We therefore performed this study to investigate whether the use of contrast material has an effect on the detection of new or enlarged MS lesions and, consequently, the assessment of interval progression.

*The private 3T scans are much more able to see the lesions that the inappropriate 1.5T scanner cannot see.

The higher resolution scans cancel out the distortions and signal noise that hide the lesion and make the scan look normal.

1.5T MRI scanners are not fit for purpose in discovering brain lesions and inflammation.

Brain lesions and inflammation, especially in the temporal lobe are responsible for poor drug response and in some cases for diagnosis.

1.5T scans are responsible for false negative (normal) brain images.

EXAMPLE OF MISDIAGNOSIS

A woman who was told she had anxiety was later diagnosed with Autoimmune Basal Ganglia Encephalitis, a rare brain condition.

When Evie Meg, 23, was a teenager, she began to suffer bouts of panic and psychosis, and was diagnosed with anxiety disorder by doctors.

Meg began experiencing seizures when she was 17, along with temporary limb paralysis that left her unable to walk for a month, but was still told that it was due to anxiety.

Frustrated with the diagnosis, the then-teenager began sharing her symptoms and experiences on TikTok, where she was reached out to by a concerned follower.

“I posted a video of me walking across my kitchen without crutches, just taking a few steps,” Meg explains. “That video went viral and the support from it was amazing. People were saying how proud they were that I’d learnt to walk again. It just went from there, really.

“In 2021, I started getting loads of messages from this girl who had been commenting on all of my TikTok videos, saying I should look into this condition. She had it and she was so convinced that I had it.”

Because of this interaction, Meg booked in to see a specialist who diagnosed her with the brain inflammation disorder.

“When I got the diagnosis, we’d had to go private to find a specialist,” Meg says. “The NHS just don’t know what to do with me, because it’s such a complex and unusual condition.

“I have daily seizure activity. I have really severe pain above my right eye, and I haven’t been able to walk properly since May 2023. I get a lot of tiredness. It affects my mood quite a lot as well, I can get really upset or angry for no reason.”

Meg says she was put on antibiotics and steroids upon diagnosis, which stopped her seizures.

“It was crazy how quickly things turned around. I couldn’t believe it,” she adds. “We stayed with the doctors in London for a while, but I started becoming resistant to the antibiotics.

“Because my condition was not diagnosed for such a long time, it was allowed to progress and get a lot worse. It means it’s much more difficult to treat now, so we had to look for more intense options.”

Meg adds that her mum began researching the infusions that she needed and found a clinic in Poland that offered them – but at at £20,000 price tag.

“Last year, when I went to Poland for tests, they found loads of other infections in my blood, which could be causing the brain inflammation,” she adds.

“The SOT I had in January was to treat one of the infections, but we’re very early days – we’ve got to treat each one individually. Because they found so many, they have to do it multiple times to treat each infection. The next year or so for me is looking like a lot more SOT infusions – but I’m taking it one day at a time.”

Meg and her family have begun a fundraising campaign to help her have the treatment she needs, and have raised over £16,000 so far.

“The support has been pretty insane,” she says. “We had a local fundraiser in a church hall, and we raised over £4,000 just doing tombolas and raffles in that one afternoon.

“It’s been incredible – very overwhelming but in the best way. I became a lot more passionate about raising awareness when I got my correct diagnosis, because it just showed how it can be missed so easily. I really want people to know that and see that so that other people don’t go through what I did.”

Autoimmune Basal Ganglia Encephalitis is estimated to affect just 1.5 in every 100,000 people in England, and is characterised by the rapid development of akinesia, rigidity, and tremors.

It is a form of Encephalitis, which the NHS says is “an uncommon but serious condition in which the brain becomes inflamed”. The very young and the very old are the age groups most at risk.

Some symptoms of Encephalitis include seizures and fits, confusion, disorientation, changes in personality or behaviour, difficulty speaking, and weakness or loss of movement in parts of the body.
It adds that causes are not always clear but, rarely, it can be caused by common viruses such as herpes simplex (cold sores), or chickenpox spreading to the brain; a problem with the immune system; or bacterial or fungal infections. And in Elizabeth’s case she contracted Covid twice at Ash Villa.

It is possible for some people to make a full recovery from Encephalitis, but the NHS says this can be a ‘long and frustrating’ process.

Additional reporting by SWNS.

Antipsychotics and the brain
Neuro-imaging research (MRI scans) of the brains of people under psychosis reveal changes in brain activity. Some of these changes may be linked to the psychosis vulnerability itself (or to environmental risk factors that increase psychosis vulnerability, such as trauma), but many of these changes are clearly also related to several non-specific, external, factors, such as antipsychotics, smoking, obesity and drug use.

Animal tests have confirmed that antipsychotics indeed contribute to changes in the brain. The question remains, however, whether the changes in the brain caused by antipsychotics can also be linked to the specific risks. Also unknown is in how far these effects are permanent.

Antipsychotics and negative symptoms
Antipsychotics work by making people somewhat indifferent. This lowers the ‘importance’ or ‘significance’ of their psychosis, sometimes to the point where the symptoms fade away completely. The problem is, however, that this medicine-induced indifference does not only affect the psychosis, but every personal emotion or experience. The suppressing of emotions makes the user of antipsychotics more numb and less active. The extent to which this happens is different from person to person, but some are seriously impaired by it.

This indifference is also called ‘secondary negative symptoms’. That term is confusing however, because it is impossible to make a distinction between the primary symptoms (caused by psychosis) and the secondary symptoms (caused by the antipsychotics).

In practice, the rule should be: negative symptoms (indifference, inaction) must be attributed to the antipsychotics unless proven otherwise.
In other words: these symptoms require treatment, and should not be regarded as a consequence of psychosis when the real cause is the medication.

Can antipsychotics make psychosis worse? Dopamine supersensitivity syndrome (DPS)
When taking antipsychotics over a long time, the body will try to compensate the effects of the medication. Because antipsychotics work by blocking the dopamine receptor D2 in the brain, the body responds by trying to remove this blockade some way or another. As early as in the 1960’s, the scientist Chouinard described how this can cause “supersensitivity” in the dopamine D2 receptor. As such, the eventual effect can be an increase of psychosis sensitivity instead of the expected decrease.

Symptoms of dopamine supersensitivity syndrome:
Abnormal movements – also called tardive dyskinesia
Increased psychosis vulnerability
Increase of the dosage required to suppress psychosis
More psychotic symptoms after stressful events.

Although the existence of DPS is not yet proven beyond doubt, it has become an issue of growing importance in practice. Some studies suggest that people who reduce medication, or quit altogether, have a higher risk of relapsing into psychosis in the first years (possibly due to the now ‘supersensitive’ D2 receptor). Yet on the longer term (when the ‘supersensitive’ receptor has returned to normal), they are better off than people who remain on their regular high dose.

Many psychiatrists are still unfamiliar with DPS
It is important to recognise DPS in an early stage. Otherwise people can end up with huge doses of antipsychotics, while still only highly increasing the risk of psychosis. T.

Conclusion: antipsychotics and dopamine
The perspectives on antipsychotics are rapidly changing. Anyone using antipsychotics, should in any case take the risk of DPS into account. Doctors prescribing antipsychotics should do the same. From the very first start of using antipsychotics, an accompanying strategy is required for reducing the dosage to its minimum, out of concern for the physical health and the effects on the brain. Sound alternatives are dopamine receptor partial agonists.

It is so disturbing the way the MH try to avoid essential scans and dismiss cancer and other neurological conditions without looking into it. Another shocking area is Enfield and also I am in touch with shocking cases in Weston – both areas only have a 1.5 Tesla by the way.