Friday, 12 July 2013

Liverpool Care Pathway - Experimentally My Dear Ellershaw

Such a possibility of possibilities...
Such a possibility of possibilities...
Such a possibility of possibilities...

Jeremy Hunt -

The Express

a man obsessed or a man inspired?

The government review is shortly to make its learned deliberations known.

The government inquiry is under way, currently recruiting suitable subjects for death road in the Flemish killing wards.

Dave Cameron has set his Dementia CQUIN targets and the bounty hunters are out.

Is the inquiry to be a model, perhaps, for research into Dementia...?

Is this why Mr. Hunt speaks with such confidence? Such a surfeit of subject material for productive investigation and clinical trials...

They want you! They want you!
They want you as a new recruit!

They want you! They want you!
They want you as a new recruit! 

Medical opinion was that you didn't die of Dementia but rather the effects of Dementia. That was before Dementia was redefined as a terminal illness.
Dementia is not a single illness but a collection or consequence of many, including Parkinson's disease, vascular dementia and Alzheimer's disease (which accounts for some 70% of all dementia cases). In the advanced stages of dementia, it is often impossible to tell which disease the patient had at the outset, as the end result is the same, according to Mitchell's study: a syndrome of symptoms and complications — eating problems (86%), pneumonia (41%), difficulty breathing (46%), pain (39%) and fever (53%) — caused by brain failure. "Dementia ends up involving much more than just the brain," says Dr. Claudia Kawas, professor of neurology at the University of California, Irvine. "We forget the brain does everything for us — controls the heart, the lungs, the gastrointestinal tract, the metabolism."Time
Anti-psychotic drugs are used in the treatment of dementia. 
At some point in the course of their illness, 90% of those with dementia are expected to develop significant behavioral problems. Behavioral disturbances occur throughout the course of dementia, irrespective of level of cognitive impairment.

Although cognitive disturbances have received the most attention in terms of targeted pharmacotherapy in patients with dementia, behavioral disturbances are a source of considerably more morbidity and are also more amenable to pharmacotherapy. Patients with dementia and behavioral disturbances behave in a manner that may place themselves and others in danger, contribute to a great deal of distress and burden for caregivers, and severely disrupt family, social, and institutional networks. Behavioral disturbances are frequently reasons for acute hospitalization and long-term institutional placement. Behavioral disturbances associated with dementia may lead to caregiver “burnout” and a decrease in empathy. Behavioral disturbances are one of the primary reasons why health care professionals are asked to intervene. Early recognition and prompt treatment of behavioral disturbances will go a long way toward improving quality of life of patients and their families and caregivers and reducing health care costs.
- National Center for Biotechnology Information
'Quality of life' and palliative care is more often the focus.
The fact that Mum had dementia and limited mobility has been mentioned a few times, and now it is mentioned again. Was this the criteria used to decide that all active treatment should be withdrawn?Mail Online
The LCP has been busy about its business.


We can do better than euthanasia. This is an opportunity not to be missed.

What if? The scientific possibilities! The scientific possibilities!

And such a possibility of possibilities.

With funded research, the pharmaceutical companies are hunting down a copyright bounty.

Interestingly, the Telegraph reports that -

Recent research has focused on two pathological changes that take place in the brains of Alzheimer’s sufferers. The first is the deposition of amyloid plaques – lumps of protein that form in neurones and stop them working properly. The second is the build-up of “neurofibrillary tangles” caused by another abnormal protein, the tau protein.

Subsequently, beginning in 1994, published reports of cysts of Borrelia burgdorferi began to appear in the peer reviewed literature, and to date more than 40 articles from workers in Europe and the United States have ratified the scientific validity of rounded cystic forms of the spirochete emerging from the corkscrew forms under conditions of adversity (starvation, osmolar shock, acid pH, and antibiotic effects) [2]. 

Alzheimer’s disease associated with corkscrew shaped Borrelia spirochetes in autopsy brain tissue has been reported by two pathologists [3–6], but cystic forms of Borrelia burgdorferi in Alzheimer brain tissues have only been the focus of research for one pathologist in the world [7].  

Cystic profiles of borrelia closely correspond to the diverse profiles of plaques, namely they are always round, and are capable of increase in size from little to big as cystic spirochetal growth progresses. Maturation of cysts parallels ‘‘maturation’’ of plaques of increasing age, based on observations of spirochetal cysts in a tissue culture model. Cystic spirochetes in tissue culture incorporate injured cells into their interior regions. Amyloid fibrils within blood vessels of the brain may wind up within the plaque region, now redefined as spirochetal cyst ‘‘territory’’, merely because the rounded cyst ‘‘landed on a blood vessel’’ which contained amyloid in its wall. DNA hybridization methods demonstrate the areas where Borrelia DNA is deposited in the Alzheimer brain. Hybridizations using DNA from the spirochete develop a ‘‘map’’ of the terrain of the brain where, like little rounded villages and cities, rounded ‘‘map sites’’ of spirochetal DNA appear. Spirochetal sites on these ‘‘DNA maps’’ match the sites of the plaques in the Alzheimer brain. Now is the time for a new opportunity to re-evaluate Alzheimer’s disease with DNA mapping methods.

Currently, there is no iterated model to explain, in the absence of the cystic pathway to plaque formation in AD, a mechanism to define the facts that plaques in AD are virtually always round in contour, variable in diameter and separated by neural tissue that is ‘‘plaque free’’, in the planes of histological section.

If ‘‘bad human DNA’’ is responsible for the origin of Plaques in AD, the chronology, topography, and ontogeny of plaques should be monotonous in image profiles, with all plaques emerging from a common morphology, and all plaques showing the same maturation sequence. In practice, plaques in AD are diverse in morphology and heterogeneous in maturation (as would be expected in maturation of spirochetal cysts). Diversity and heterogeneity are the ‘‘stuff’’ of cystic spirochetes.

Cyst forms, intruded into brain tissue, as a consequence of chronic infection, would solve the puzzle of the origins of the plaques.

PubMed have the abstract of this article here.

The full article is here.

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