Mad Cow Disease and When to Refer On

[Guest guest]

Hello people,

 

Thought the following might be of use in setting straight some of the

neurological information that is needed to address the question.

 

However I'll leave that to others to discuss. But it leads me to another

question relating to clinical experience and practise:

 

When do you refer on cases to other practitioners for further treatment? What

motivates your decision/s to do so? And, perhaps most importantly, what do you

see as being the limitations of ?

 

 

Cheers,

Jay.

 

 

Quoting from " Clinical Neurology 5th ed " (Greenberg, Aminoff & Simon) -

McGraw-Hill - 2002:

 

" Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob Disease (CJD) is an invariably fatal transmissible disorder of

the central nervous system characterised by rapidly progressive dementia and

variable focal involvement of the cerebral cortex, basal ganglia, cerebellum,

brainstem and spinal cord. The annual incidence is about 1:1,000,000 population.

The naturally aquired disease occurs in patients 16-82 years of age with a peak

incidience between 60 and 64 years and an equal sex incidence.......

Although transmission from humans to animals has been demonstrated

experimentally, documented human-to-human transmission (by corneal

transplantation, cortical electrode implantation, or administration of human

growth hormone) is rare. The infectious agent is present in the brain, spinal

cord, eyes, lungs, lymph nodes, kidneys, spleen, liver, and CSF, but not other

body fluids.

 

Pathogenesis

A proteinaceous infectious particle (prion) is the etiological agent.

Familial cases, which are uncommon, have been associated with mutations in the

form of the prion protein (cellular isoform PrPsc) that is expressed by normal

neurons, but whose function is unknown... ,the result is accumulation of

abnormal PrPsc prions in the brain. To explain the ability of of PrPsc prions to

replicate in the brain (despite the fact that they contain no detectable nucleic

acids), it has been suggested that infectious PrPsc prions induce a

conformational change in normally expressed PrPsc prions that converts them to

the PrPsc form.

....

 

Clinical Findings

The clinical picture may be that of a diffuse central nervous system

disorder or of a more localized dysfunction. Dementia is present in virtually

all cases and may begin as a mild global cognitive impairment or a focal

cortical disorder such as aphasia, apraxia or agnosia. Progression to akinetic

mutisim or coma typically ensues over a period of months. Psychiatric symptoms

including anxiety, euphoria, depression, labile affect, delusions,

hallucinations and changes in personality or behaviour may be prominent.

Aside from cognitive abnormalities, the most frequent clinical

manifestations are myoclonus ... extrapyrimidal signs, ... and cerebellar signs.

Visual field defects, cranial nerve palsies, and siezures occur less often.

A distinct variant of CJD is thought to result from the transmission of

bovine spongiform encephalopathy (BSE - " mad cow disease " ) to humans.This

variant is characterised by earlier onset (mean age, about 30yrs), a more

prolonged course (greater than 1 year), invariable cerebellar involvement,

prominent early psyhciatric abnormalties, and diffuse amyloid plaques.

.....

Prognosis

No treatment is currently available. The disease is usually relentlessly

progressive and, although transient improvement may occur, is invariably fatal.

In most sporadic cases, death occurs within one year after the onset of

symptoms: the mean duration of illness in these patients is 7 months. "

 

 

 

twomtns2002 <twomtns2002 wrote:

This disease has an important factor in todays diagnosis. It is a

taboo subject and like aids, people have died of it and it has been

listed as something else. It has been proliferated at an extent that

can only mean premeditative intent. It is an international crime.

Little has been published, but we can assume that there is no cure.

Mad Cow disease is a disease that is self ingested. I think an

enzyme of some sort is manufactured in the stomach/liver area. It is

not filtered by the kidneys and affect the brain in the area of the

Gall Bladder meridian. Ha fau chi. How to treat this disease in TCM?

I have has neither a patient or any reports that I have read. I have

seen television of the poor cows. Spastic head movements and loss of

ability to direct tongue movements charachterize the disease. One of

the common symptoms is a lightheadednes after eating beef or dairy

products. One of the first symptoms is loss of control of the

tongue. What would I try if I could?

 

I think there is an overabundance of moisture in the body. Balance

is affected. The bad moisture is the acids that are created. They

seem to destroy brain tissue. Could a process of depriving the

patient of fluids, and supplemented with a process similar to

donating plasma be used? I think the white cells are affected the

most. Perhaps even transfusion would work. These fluids taken out

would be contaminated. The following points might work in a

beginning stage of the disease. That down side being the patient may

never regain brain abilities even if saved from death.

Massage may help these patients and if in the advanced stages of the

disease they would probably move around too much for needles.

 

Massage and Tonify the heart

 

Moxa kidney knee area.

 

Sedate the stomach hand area

 

tonify and moxa Gall Bladder head, I can see four or five moxa

needles up there

 

Trying to tonify or sedate the brain tissue would seem to be a good

step if possible. Stopping the growth of the enzyme reaction might

have a herb helper? Hot chinese mustard? Other brain food?

Cauliflower?

 

 

ahoo! Groups Sponsor

 

 

 

 

 

 

Want to chat instantly with your online friends? Get the FREE Messenger

 

 

[Guest guest]

Isn't lightheadedness after dairy also a symptom of allergy and other things?

Michelle

-

jay mackley

Chinese Traditional Medicine

Tuesday, August 05, 2003 5:23 AM

[Chinese Traditional Medicine] Re: Mad Cow Disease and When to Refer On

 

 

Hello people,

 

Thought the following might be of use in setting straight some of the

neurological information that is needed to address the question.

 

However I'll leave that to others to discuss. But it leads me to another

question relating to clinical experience and practise:

 

When do you refer on cases to other practitioners for further treatment? What

motivates your decision/s to do so? And, perhaps most importantly, what do you

see as being the limitations of ?

 

 

Cheers,

Jay.

 

 

Quoting from " Clinical Neurology 5th ed " (Greenberg, Aminoff & Simon) -

McGraw-Hill - 2002:

 

" Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob Disease (CJD) is an invariably fatal transmissible disorder

of the central nervous system characterised by rapidly progressive dementia and

variable focal involvement of the cerebral cortex, basal ganglia, cerebellum,

brainstem and spinal cord. The annual incidence is about 1:1,000,000 population.

The naturally aquired disease occurs in patients 16-82 years of age with a peak

incidience between 60 and 64 years and an equal sex incidence.......

Although transmission from humans to animals has been demonstrated

experimentally, documented human-to-human transmission (by corneal

transplantation, cortical electrode implantation, or administration of human

growth hormone) is rare. The infectious agent is present in the brain, spinal

cord, eyes, lungs, lymph nodes, kidneys, spleen, liver, and CSF, but not other

body fluids.

 

Pathogenesis

A proteinaceous infectious particle (prion) is the etiological agent.

Familial cases, which are uncommon, have been associated with mutations in the

form of the prion protein (cellular isoform PrPsc) that is expressed by normal

neurons, but whose function is unknown... ,the result is accumulation of

abnormal PrPsc prions in the brain. To explain the ability of of PrPsc prions to

replicate in the brain (despite the fact that they contain no detectable nucleic

acids), it has been suggested that infectious PrPsc prions induce a

conformational change in normally expressed PrPsc prions that converts them to

the PrPsc form.

....

 

Clinical Findings

The clinical picture may be that of a diffuse central nervous system

disorder or of a more localized dysfunction. Dementia is present in virtually

all cases and may begin as a mild global cognitive impairment or a focal

cortical disorder such as aphasia, apraxia or agnosia. Progression to akinetic

mutisim or coma typically ensues over a period of months. Psychiatric symptoms

including anxiety, euphoria, depression, labile affect, delusions,

hallucinations and changes in personality or behaviour may be prominent.

Aside from cognitive abnormalities, the most frequent clinical

manifestations are myoclonus ... extrapyrimidal signs, ... and cerebellar signs.

Visual field defects, cranial nerve palsies, and siezures occur less often.

A distinct variant of CJD is thought to result from the transmission of

bovine spongiform encephalopathy (BSE - " mad cow disease " ) to humans.This

variant is characterised by earlier onset (mean age, about 30yrs), a more

prolonged course (greater than 1 year), invariable cerebellar involvement,

prominent early psyhciatric abnormalties, and diffuse amyloid plaques.

....

Prognosis

No treatment is currently available. The disease is usually relentlessly

progressive and, although transient improvement may occur, is invariably fatal.

In most sporadic cases, death occurs within one year after the onset of

symptoms: the mean duration of illness in these patients is 7 months. "

 

 

 

twomtns2002 <twomtns2002 wrote:

This disease has an important factor in todays diagnosis. It is a

taboo subject and like aids, people have died of it and it has been

listed as something else. It has been proliferated at an extent that

can only mean premeditative intent. It is an international crime.

Little has been published, but we can assume that there is no cure.

Mad Cow disease is a disease that is self ingested. I think an

enzyme of some sort is manufactured in the stomach/liver area. It is

not filtered by the kidneys and affect the brain in the area of the

Gall Bladder meridian. Ha fau chi. How to treat this disease in TCM?

I have has neither a patient or any reports that I have read. I have

seen television of the poor cows. Spastic head movements and loss of

ability to direct tongue movements charachterize the disease. One of

the common symptoms is a lightheadednes after eating beef or dairy

products. One of the first symptoms is loss of control of the

tongue. What would I try if I could?

 

I think there is an overabundance of moisture in the body. Balance

is affected. The bad moisture is the acids that are created. They

seem to destroy brain tissue. Could a process of depriving the

patient of fluids, and supplemented with a process similar to

donating plasma be used? I think the white cells are affected the

most. Perhaps even transfusion would work. These fluids taken out

would be contaminated. The following points might work in a

beginning stage of the disease. That down side being the patient may

never regain brain abilities even if saved from death.

Massage may help these patients and if in the advanced stages of the

disease they would probably move around too much for needles.

 

Massage and Tonify the heart

 

Moxa kidney knee area.

 

Sedate the stomach hand area

 

tonify and moxa Gall Bladder head, I can see four or five moxa

needles up there

 

Trying to tonify or sedate the brain tissue would seem to be a good

step if possible. Stopping the growth of the enzyme reaction might

have a herb helper? Hot chinese mustard? Other brain food?

Cauliflower?

 

 

ahoo! Groups Sponsor

 

 

 

 

 

Want to chat instantly with your online friends? Get the FREE Messenger

 

[Guest guest]

> Thought the following might be of use in setting straight some of

the neurological information that is needed to address the question.

 

Thanks, Jay for the background on Creutzfeldt-Jakob Disease. One

thing I want to add is the danger of feeding ground-up animals to

other animals.

 

> When do you refer on cases to other practitioners for further

treatment? What motivates your decision/s to do so? And, perhaps most

importantly, what do you see as being the limitations of Chinese

Medicine?

 

I'll leave the first part of your question to the clinical

practitioners on the list. In general, Western allopathic medicine

and public health measures are best for trauma and parasite control.

Public sanitation can play a big role in bringing parasitic

infections under control via prevention. Chinese medicine often is

best for chronic conditions. In some cases (like some serious blood

disorders like leukemia) the combination of Western and Chinese

medicine works better than either alone. This is not saying that

there are not TCM treatments which can help in cases of trauma and

parasitic infection or that Western allopathic and in particular

Western alternative medicine don't have serious contributions to make

in the treatment of chronic disorders. These are generalities.

 

Victoria