Category: Illness or disabilaties
Introduction and description
Parkinson's disease is a degenerative disorder of the central nervous system. It is essentially brain damage which appears to start in the region of the brain stem. The disease is characterised by the accumulation of a protein called alpha-synuclein into inclusions called Lewy bodies in neurons. The disease then spreads and gradually kills off or disrupts the function of more of the parts of the brain.
Parkinson's disease is believed to affect between 1 and 1.5 million Americans. Each year, 50,000 Americans are diagnosed with Parkinson's disease. The figure is increasing.
The map shows incidence of Parkinson's disease, measured in ‘disability-adjusted life years’ per 100,000 inhabitants in 2004. The so called developed nations bear the biggest burden with an interesting additional burden borne by oil rich countries. PD is the second most common neurodegenerative disorder after Alzheimer's disease. The prevalence (proportion in a population at a given time) of PD is about 0.3% of the whole population in industrialised countries. Prevalence rises from 1% in those over 60 years of age to 4% of the population over 80. The mean age of onset is around 60 years, although 5–10% of cases, classified as young onset, begin between the ages of 20 and 50.
Parkinson’s disease is classified by its symptoms rather than its cause. As such it is helpful first to look at the main symptoms by which the disease is diagnosed and the 'progress' of the disease.
One of the first symptoms to manifest in Parkinson’s disease is tremour. Characteristics may include a rhythmic shaking in the hands, arms, head, legs, or trunk; shaky voice; difficulty writing or drawing; or problems holding and controlling utensils, such as a fork. But not all tremours are caused by Parkinson’s disease and there do seem to be some incidences of misdiagnosing, which lead to the prescribing of drugs which only serve to make a person unwell who was not that ill.
I have provided a section in the science section showing all the alternative possible causes of tremour - all of which should be investigated before a diagnosis of Parkinson's disease is made.
The only way to diagnose Parkinson's disease is not by the symptom of the tremour but by a brain scan. If it is, indeed, Parkinson’s disease the brain scan will show that there is destruction of parts of the hindbrain. Although the medulla may be unaffected, the pons and reticular formation are. Fluctuations in attention and slowed cognitive speed are among many early cognitive difficulties. Sleep patterns may be disrupted - see the Brain and its functions.
The next symptoms which seem to develop and become more obvious relate to movement problems including shaking, rigidity, slowness of movement and difficulty with walking and gait. In effect the pathogen is moving up the brain stem, spreading and causing more damage. Yet again, these symptoms can manifest in the old and people with other diseases, but at this stage there are quite clear indications of the differences.
The Midbrain is the smallest region of the brain that acts as a sort of relay station for auditory and visual information. Portions of the midbrain called the red nucleus and the substantia nigra are involved in the control of body movement.
The cerebellum - lies on top of the pons, behind the brain stem. It too is involved in the coordination of motor movements. The tasks where the cerebellum most clearly comes into play are those in which it is necessary to make fine adjustments to the way an action is performed.
|Damage to the cerebellum is more long term than damage to other areas and there is less evidence that the damage spreads to this area that quickly.|
Other recognized motor signs and symptoms include gait and posture disturbances such as ‘festination’ - rapid shuffling steps and a forward-flexed posture when walking.
Most of these symptoms are an indication that the pathogen is progressing up the spinal column, but some of them indicate that the disease has started to disrupt the centres of learnt function. Functions such as tying shoelaces and riding bicycles or walking are all learnt functions and laid down at an early age. Thus the earlier learnt functions may be the first to be disrupted – which is why the person has more difficulty walking, than riding a bike.
The disruption does not necessarily mean the function itself has been destroyed, it may simply mean the processor which executes the function has been damaged. There are may positive areas of research at the moment concentrating on the mind's ability to relearn function - which can then be stored elsewhere - see the Brain as hardware.
The next stage can be sensory problems such as loss of the sense of smell. This is then an indicator that the damage has spread to the thalamus – see Brain and its functions.
The thalamus is located above the brainstem, and processes and relays movement and sensory information. It is essentially a relay station, taking in sensory information and then passing it on to the cerebral cortex.
Damage here knocks out sensory information and contributes to sensory deprivation. It is at this stage that hallucinations start to appear. If the sense of smell is damaged, the person can get hallucinations of smell. Any damage to the hearing produces auditory hallucinations and damage to the senses of touch produce odd inexplicable sensations such as those of tingling or pins and needles.
All of these are fairly common in the later stages of Parkinson’s disease, although it is clear that some hallucinations are caused by the medication given to patients.
I addition to the sensory hallucinations mentioned, people with Parkinson’s disease can get visual hallucinations. Damage to the thalamus can produce temporary lapses of processing of the output to the occipital region, during which visual hallucinations occur. The eye, and the occipital region are undamaged. The eye sends information to the thalamus which then sends it on to the occipital region to be processed, but the damage to the thalamus can result in temporary disruptions, which then result in ‘waking dreams’.
These waking dreams are totally real to the person. They can be hallucinations in which the images from the composer are superimposed over the input from the eye, or they can be true visions in which nothing from the eye gets through and the result is entirely based on information from the composer.
PD versus Dementia
In the descriptions of the stages of Parkinson’s disease one often sees the statement that “Dementia, occurs in advanced stages of PD”. What makes the advance of the disease different however, is that it is not true dementia because the advance of the disease is in the reverse order to dementia itself. In dementia, the spread of brain damage goes from the frontal lobe of the cerebral cortex and gradually goes inwards towards the limbic system. It rarely reaches the brain stem.
In contrast, the spread of degeneration in Parkinson’s disease is from the brainstem upwards and outwards as such the frontal lobes and parietal lobes are some of the last regions to be affected.
The parietal lobe is located in the middle section of the brain and is associated with processing tactile sensory information such as pressure, touch, and pain. People with dementia tend to experience pain a good deal less than normal because this centre gets destroyed fairly early on.
But Parkinson’s disease appears to leave the parietal lobe intact until very late on. As such people with Parkinson’s disease can suffer pain. This needs to be borne in mind, as their unsteadiness makes them subject to falls. Considerable help is needed to make sure they are not hurt in any way.
They may also start to lose control of their bladder and may suffer both diarrhoea and constipation - but again the medications do not help here. It is not unusual for the medications to be the cause of these problems and not the disease.
Deafness and understanding problems
The next set of symptoms to develop are related to damage of the temporal lobe, again see Brain and its functions.
The temporal lobe is located on the bottom section of the brain. This lobe is also the location of the primary auditory cortex, which is important for interpreting sounds and the language we hear. Visions, Hallucinations and other spiritual experiences become much stronger at this stage.
The medial temporal lobe (MTL) becomes activated during Memory recall. As the patogen progresses, it is this region that goes next and here we see that many learnt functions get destroyed or become inaccessible. Because behavioural functions are the first to be laid down in Memory, it is often behavioural functions that go first.
Behavioural functions control our learnt behaviour in reaction to stimuli. They are a means of controlling emotional outbursts, as well as conforming to the norms of society. As such, any loss of behavioural function results in uncontrolled Emotion and activity 'outside societal norms'.
At this stage therefore the person may turn very gradually into an uncontrollable child. They can be rude, outspoken, with outbursts of anger and frustration, they may cry, laugh hysterically, or worse. One sufferer I know used to fart for fun. He also made rude gestures to anyone he felt like, and threw his food on the floor when he didn’t like it. Unfortunately a 60 to 80 year old person behaving like a child is nowhere near as endearing as a real child and the tantrums and emotional behaviour is often seen as extremely upsetting for those witnessing it - unless of course you understand why.
We have a tendency to forget just how much of our behaviour – particularly in the so called ‘developed countries’ – is controlled. We control it in order to be able to live and work effectively together and of course it works, we have achieved huge amounts by being behaviourally controlled, polite and restrained. Politics is just learnt behaviour of a very extreme and largely manipulative sort. When this sort of learnt function goes, we see the person ‘in the raw’, it can be a huge shock for relatives and friends. Nursing staff tend to be used to it.
Since there are no curbs on their behaviour, anything still going through the person’s mind will not be controlled by behavioural norms, so for example, sexual thoughts may result in sexual actions. Men need to be watched at this stage, they may be 80, but ......
Hallucinations and visions can be extremely prevalent at this time, which again makes things difficult for their relatives because they react to the visions and hallucinations as if they were ‘real’. The answer is to treat them as real too. You can enter into some quite wonderful worlds through a Parkinson's disease sufferers travels to the great beyond.
All this time, the cerebral cortex and the frontal lobe has been left relatively unscathed and you may find the person attempting to do the most bizarre things using their Reasoning function but without the necessary facts in Memory to do it.
They may attempt to repair TVs that work by taking them to bits entirely. You may come home to find the entire TV laid in bits across the living room floor.
They may try to cook a meal composed entirely of meat dripping and bread by putting it in a hot oven then leaving it and forgetting about it; or go for a walk without map, raincoat or their glasses – then get lost and become so fatigued they go to sleep in someone’s front garden [these are all true stories].
They are thus a real danger to themselves [and others] because they are essentially irrational. It is this stage that most carers of those with Parkinsons's find the most difficult, because they are unpredictable. You need all the help you can get at this stage if you are a carer, if only to give you a break and a rest.
The final stages
Any number of things can happen next. Sometimes the disease manages to progress as far as the frontal lobe affecting Reasoning ability as well, but it is more common for the disease to start to attack the central processing unit of the brain.
Thus at this stage the person dies. Release - home.
The following are now emerging as the causes of Parkinson's disease. Note the word causes. In the end something - virus, parasite, bacteria, food stuffs, toxins, lead, mercury, fungi, pharmaceuticals, has managed to get past the blood brain barrier or entered the lymph system or cerebrospinal fluid and is now in the brain cavity. The lesions are caused by an external agent - and this is key because in order to halt the progress of the disease you have to find what has found its way in there. There are no magic bullet cures, but if you know the enemy, you at least have a better chance of helping your defence forces in the fight against it.
Where not long ago links to viruses as the cause were tenuous, more autopsies on Parkinson's disease sufferers brains are revealing a host of viruses that could be implicated. It has been known for some time that the Influenza A was one cause:
Although much is known regarding the molecular mechanisms leading to neuronal cell loss in Parkinson's disease (PD), the initiating event has not been identified. … We present immunohistochemical data indicating the presence of influenza A virus within the substantia nigra pars compacta (SNpc) from postmortem PD brain sections. Influenza A virus labeling was identified within neuromelanin granules as well as on tissue macrophages in the SNpc. Further supporting a role for neuroinflammation in PD was the identification of T-lymphocytes that colocalized with an antibody to caspase-cleaved Beclin-1 within the SNpc. The presence of influenza A virus together with macrophages and T-lymphocytes may contribute to the neuroinflammation associated with this disease. PMID: 21655265
many other viruses are now also starting to be implicated, for example, the Epstein Barr virus:
A novel hypothesis of Parkinson's pathogenesis, articulated by Braak and colleagues, implicates a pathogen acting in the olfactory mucosa and gastrointestinal tract as the inciting agent. In this point-of-view article, we hypothesize that α-synuclein aggregation in Parkinson's disease is an Epstein-Barr virus (EBV)-induced autoimmune phenomenon. … Consistent with the Braak's proposed pattern of spread, we contend that axon terminals in the lamina propria of the gut are among the initial targets, with subsequent spread of pathology to the CNS. PMID: 24726430
We report on a high level of octapeptide matching between HCV, HIV-2, MPV, MUV, EBV, HHV-6, and CMV, and human brain antigens that, when altered, have been specifically associated with neuropathologies such as amyotrophic lateral sclerosis, spinocerebellar ataxia, frontotemporal degeneration, Huntington disease, Parkinson disease, cognitive impairment, aphasia and oculomotor apraxia. PMID: 24521198
We evaluated the association of HSV-1, HHV-6, and VZV with Alzheimer's disease (AD) and Parkinson's disease (PD). Brain specimens for viral DNA polymerase chain reaction represented 34 patients with AD, 40 with PD, and 40 controls. One AD patient (2.9%) was positive for HSV-1 DNA, 88.2% for HHV-6 DNA, and 26.5% for VZV DNA; 17.5% of PD patients were HSV-1 DNA-positive and 75% HHV-6-positive, whereas 40% had VZV DNA. Twenty-five percent of the controls were positive for HSV-1 DNA, 87.5% for HHV-6, and 27.5% for VZV. HSV-1, VZV, or HHV-6 DNA in brains was no additional risk factor for AD. PMID: 12891684
OBJECTIVE: To test for the presence of herpesviruses in postmortem brain samples from multiple sclerosis patients and controls using polymerase chain reaction.
METHODS: Active and inactive plaque tissue, unaffected white matter (WM) and gray matter (GM) from MS cases, and WM and GM controls (Alzheimer's disease, Parkinson's disease and non-neurological disease) were screened for the herpesvirus by PCR.
(1) 37% of the MS cases were positive for herpes simplex virus (HSV). Twenty-eight percent of controls cases were positive for HSV. Forty-one percent of active plaques were positive for HSV in contrast to only 20% of inactive plaques (Sanders et al, 1996).
(2) 57% of the MS cases and 43% of the control cases were positive for HHV-6. Thirty-two percent of the active plaques contained HHV-6 compared to 17% of inactive plaques.
(3) 43% of the MS cases and 32% of the control cases were positive for VZV. Fourteen percent of the active plaques and 10% of the inactive plaques were positive for VZV.
(4) 27% of MS cases and 38% of control cases were positive for EBV. Five percent of the active plaques were positive for EBV and 10% of the inactive plaques were positive.
(5) 16% of the MS cases and 22% of the controls were positive for CMV. Nine percent of the active plaques and 10% of the inactive plaques were positive. We also compared MS WM and GM with controls and found no significant difference. PMID: 8799216
So if we summarise, brain damage of all sorts is caused by a whole host of viruses, and which virus it is, is quite likely to depend on when we were infected and the state of our immune systems as the virus travelled round the body, rather than any particular type of virus being especially virulent in any one disease.
When we vaccinate someone we give them a dose of a virus in the hope they will build up immunity. Where the vaccine used in the injection is a live virus, there are instances where it, although apparently vanquished by the immune system, lays low and continues to attack, albeit at a much reduced rate. One example is the herpes virus, read on:
Herpes simplex viruses types 1 and 2 (HSV-1 and HSV-2) are human neurotropic viruses that establish latent infection in dorsal root ganglia (DRG) for the entire life of the host. From the DRG they can reactivate to cause human morbidity and mortality. Although they vary, in part, in the clinical disorders they cause, and in their molecular structure, they share several features that govern the biology of their infection of the human nervous system. The biology of their ability to establish latency, maintain it for the entire life of the host, reactivate, and cause primary and recurrent disease is being studied in animal models and in humans. PMID: 24142852
This is not the only virus to do this, thus any vaccine containing a live virus carries great risk with it. ...
The zoster vaccine (trade name Zostavax) is a live vaccine developed by Merck & Co. …... The zoster vaccine is, essentially, a larger-than-normal dose of the chickenpox vaccine (Varivax, Varilrix), as both shingles and chickenpox are caused by the same virus, the varicella zoster virus (VZV).
Some of the influenza vaccines use live viruses.
As such we are giving people viruses they did not have by vaccinating them. And as we have seen viruses cause brain damage of all sorts - not just Parkinson's disease.
In some ways development of vaccines is putting the cart way before the horse and it is a runaway cart liable to do untold damage. We do not know the entirety of diseases or illnesses caused by viruses or bacteria, nor do we know precisely whether each one is eradicated by the immune system or simply lies low. To give anyone a live virus when this information is not known, carries enormous risk - and one of the risks may be that a child or adult develops brain damage.
Parasites appear to be implicated in a large number of cases of Parkinson's disease and most types of parasite are implicated. Although Linda Ronstadt contracted her Parkinson's disease from tick bites, the two most obvious culprits for most people are the parasites caught from cats, dogs and foxes. Toxoplasma gondii - The parasitic protozoan Toxoplasma gondii infects about one-third of the population of developed countries. It is carried by cats [being with cats].
Toxocara canis, cati - Toxocariasis is an illness of humans caused by larvae (immature worms) of either the dog roundworm (Toxocara canis), the cat roundworm (Toxocara cati) or the fox (Toxocara canis).
Toxocara canis and Toxocara cati are perhaps the most ubiquitous gastrointestinal worms (helminths) of domestic dogs and cats and foxes. Toxocariasis is a major cause of blindness and is known to provoke rheumatic, neurologic, and asthmatic symptoms. There is also a significant correlation between high Toxocara antibody titers and epilepsy in children.
An increasing number of pharmaceuticals are being implicated in the development of Parkinson's disease. This LINK takes you to the eHealthme website where a list of the pharmaceuticals implicated in the development of Parkinson's disease are listed.
In 2016, eHealthme completely reordered their site. This meant that every link we had provided to their data no longer worked. The links to eHealthme take you to their site but not the relevant section. Thus you can use the link, but you will need to search under ‘symptoms’ and then use the section ‘drugs causing symptoms’ to get the information.
This list is not anecdotal. It is compiled from Adverse Drug eports submitted to SEDA and the FDA.
The list is depressingly familiar with statins figuring quite highly as well as a host of frequently prescribed drugs. Drugs to treat osteoporosis, for example, reappear again and again as a cause of illness and they appear here too. Any drug that attacks the intestinal flora - such as antibiotics or that attacks the stomach acid - such as proton pump inhibitors or antacids, even aspirin are implicated in this disease plus a host of other brain diseases, because they compromise the body's natural defences. Food particles, viruses, parasites, bacteria and so on can enter the blood stream via the intestinal tract. If we take an example. One specific pharmaceutical mentionned is Metoclopramide, a medication used mostly for stomach and esophageal problems. It is commonly used to treat nausea and vomiting, in diabetes and gastroesophageal reflux disease. As at mid 2014, 720 reports of Parkinson's caused by this drug had been reported.
Current concepts regarding the pathogenesis of Parkinson's disease support a model whereby environmental factors conspire ... initiate the disease. ......There is incontrovertible evidence that aggregation of the neuronal protein alpha-synuclein is central to disease pathogenesis. A novel hypothesis of Parkinson's pathogenesis, articulated by Braak and colleagues, implicates a pathogen acting in the olfactory mucosa and gastrointestinal tract as the inciting agent. PMID: 24726430
In effect, the other source of entry is any pharmaceutical that is delivered via the nose, as the nose is a very vulnerable point of entry. One very obvious pharmaceutical delivered this way is the vaccine. The influenza vaccine used on adults and increasingly on children of all ages is delivered this way and is being promoted more and more as an alternative to the injection. We should expect to see an increase in the number of both children and adults with brain damage as a consequence of this government policy.
The other culprit may be the anti-histamine nasal spray, which by compromising the body's natural mucosa and histamine defences, opens the way for any number of viruses or similar to enter via the nasal cavity. There are literally hundreds and hundreds of Adverse Health reports from people who have developed Parkinson's from anti-histamines - see the Link. It is worth mentionning that these pharmaceuticals are often available over-the-counter without prescription.
The evidence here is very strong. Heavy metals include lead and mercury, however, iron, copper and manganese are all implicated in the formation of Parkinson's disease.
Manganese can cause manganism, an irreversible neurological disorder similar to Parkinson's disease. Exposure to manganese is usually from occupational sources - welding, mining, alloy production, ferro-manganese operations especially in which manganese ore or manganese compounds are turned into steel, and work with agrochemicals. The towns and communities surrounding the areas of manganese heavy industry can also become affected by toxic exposure to manganese.
The objective of this study was to determined if there was a relationship between Grover's disease [a skin disease] and Parkinson disease. ...Fourteen patients with Parkinson disease and 14 control patients were randomly selected and examined for cutaneous eruptions and blood mercury levels....Of the 14 patients with Parkinson's disease, 13 had Grover's disease and detectable blood mercury. None of the patients in the control group had a cutaneous eruption and only 2 of the 14 had detectable blood mercury.....Mercury may play a role in the etiology of Parkinson disease and Grover's disease. PMID: 16832218
Both lead and mercury are particulalry prevalent in the brains [and blood] of those with Parkinson's disease. Both lead and mercury are proven to produce various forms of brain damage, as such they are implicated in all sorts of other brain degeneration.
In this we should not forget the role of dental amalgam fillings, as they are mercury based. Where a filling is leaking or poor dental work has been undertaken, then the mercury may be the cause.
Nanoparticles may also be implicated. Nanoparticles are classified as a toxin, they were- invented by scientists and are being released into the environment by scientists and pharmaceutical companies in the belief that they do no harm, except that yet other researchers have realised they do a lot of harm......
....DNA damage occurs chemically or physically by nanomaterials. Chemical and physical damage are associated with point mutation by free radicals and double strand brake, respectively. The failure of DNA repair and accumulation of mutations might occur when inflammation is prolonged, and finally normal cells could become malignant. These free radicals can not only damage cells but also induce signaling molecules containing immunoreaction. Nanoparticles and asbestos also induce the production of free radicals. .... Taken together,... a variety of diseases [may be] induced by nanomaterials. PMID: 25097864
Numerous toxins are implicated in Brain damage in general. One known toxin linked to Parkinson's is Paraquat - the weedkiller.
Paraquat is a quaternary ammonium herbicide. Other members of this class include diquat, cyperquat, diethamquat, difenzoquat and morfamquat.
Pesticides are known to be associated with an increased rate of Parkinson's Disease. Paraquat structurally resembles MPTP and its metabolite MPP+. MPTP and MPP+ are neurotoxic chemicals, that induce Parkinson's Disease in exposed humans. Paraquat might therefore might, as do MPTP and MPP+ inhibit tyrosine hydroxylation, which is essential for the formation of dopamine.
from Parkinson's Disease information helpsite
Rotenone is an insecticide that has the potential to cause Parkinson's disease. Insecticides are also known to affect well water. Rotenone is commonly used in powdered form to treat parasitic mites on chickens and other fowl, and so can be found in poultry. Rotenone is produced by extraction from the roots, seeds, and leaves of certain tropical legumes. Rotenone inhibits tyrosine hydroxylation, which is essential for the formation of dopamine. So rotenone could cause Parkinson's disease by lowering dopamine levels. When given intravenously to mice, rotenone has been demonstrated to cause a model of Parkinson's disease. Rotenone toxicity is also caused by complex I inhibition, depletion of cellular and oxidative damage. These processes cause loss of midbrain dopaminergic neurons, leading to depletion of dopamine in the brain.
Maneb is a fungicide that contains manganese. The major active element of Maneb is manganese ethylene-bis-dithiocarbamate. Pesticides are known to be associated with an increased rate of Parkinson's disease, so there is a greatly increased likelihood of developing toxic symptoms by people involved in horticulture and agriculture. As Maneb contains manganese it is possible that it causes Parkinson's Disease symptoms via the same means as manganese, which is by inhibiting tyrosine hydroxylation, which is essential for the formation of dopamine. The effects of Maneb are potentiated when there is also exposure to the pesticide Paraquat
For more toxic causes follow this LINK.
There appears to be some evidence that deprivation of certain vitamins could be one cause of Parkinson's disease....
Homocysteine (Hcy) is a sulfur-containing amino acid that is generated during methionine metabolism. It has a physiologic role in DNA metabolism via methylation, a process governed by the presentation of folate, and vitamins B6 and B12.
Physiologic Hcy levels are determined primarily by dietary intake and vitamin status.
Elevated plasma levels of Hcy (eHcy) can be caused by deficiency of either vitamin B12 or folate, or a combination thereof.
...... eHcy has been observed in several medical conditions, such as cardiovascular disorders, atherosclerosis, myocardial infarction, stroke, minimal cognitive impairment, dementia, Parkinson's disease, multiple sclerosis, epilepsy, and eclampsia. There is evidence from laboratory and clinical studies that Hcy, and especially eHcy, exerts direct toxic effects on both the vascular and nervous systems. This article provides a review of the current literature on the possible roles of eHcy relevant to various neurologic disorders. PMID: 25324876
There is also evidence that overdose of vitamins and minerals via supplements can cause Parkinson like symptoms. One culprit is magnesium. The following is from eHealthme.
On Oct, 31, 2014: 11,124 people reported to have side effects when taking Magnesium. Among them, 57 people (0.51%) have Parkinson's Disease.
Fungal infections of various sorts are implicated in some cases of the disease.....
... Several mechanisms have been implicated in the etiopathogenesis of PD .... Recent research suggests that salsolinol, a derivate of dopamine, is an important contributing factor. In the presence of acetaldehyde, dopamine is converted into salsolinol, a neurotoxin involved in apoptosis of dopaminergic neurons. Increased production of acetaldehyde is associated with chronic polysystemic candidiasis (CPC). Chronically elevated levels of acetaldehyde in patients with CPC might participate in the formation of salsolinol and its metabolites in the brain contributing to the destruction of dopaminergic cells in substantia nigra. Clinical mental symptoms of PD often correspond with the mental manifestations of CPC. PMID: 17051898
There are links between certain bacteria and Parkinson's disease, although as yet this early research has not established whether the bacteria are present because of the disease or are present and cause the disease, for example
There is increased proportional mortality from Parkinson's disease amongst livestock farmers. ...... [The aim of this study was to] compare the frequency of H. suis, relative to H. pylori, in gastric biopsies of patients with idiopathic parkinsonism (IP) and controls from gastroenterology services. Relative risk of having H. suis in 60 IP patients compared with 256 controls was 10 times greater than that of having H. pylori....... Multilocus sequence testing comparison with porcine strains may clarify whether transmission is from pigs/porcine products or of human-adapted, H. suis-like, bacteria. PMID: 24117797
Both physical damage that is accidental and surgery may cause brain damage, as such there is the possibility it will also cause Parkinson's disease.
There may be other causes, as in other brain diseases there has been research that implicates Radiation and Hypoxia [caused by poor air quality] but I could find no papers on Pubmed where research has been done specifically for Parkinson's disease. Another area worth investigating may be fluoride imbalance, as again, this is implicated in some forms of brain damage.
The presence of Food allergies may be a sign that food has pentrated the intestinal wall [or has been injected via vaccines] at some stage and entered the blood stream. If it has manged to cross the blood brain barrier it will be pathogenic in its action. Thus although Food allergy is not the cause, the presence of intolerances can be a clue - the cause is then either a vaccine or food itself, depending on the food. It is relatively easy to get yourself tested for food allergies and intiolerances and even if the food is not a cause, avoiding any to which you are intolerant takes some strain from your system.
There are two approaches to the treatment of Parkinson's disease
In this the symptoms are tackled and the tendency here is to administer Parkinson's disease drugs. A recent development, where the disease has progressed is to also use nicotine patches - see the observations.
Parkinson's disease drugs can certainly relieve many people's symptoms in the relative short term and longer. However, the after effect of any stimulatory drug ends up causing an opposite after effect. So drugs for Parkinson's Disease can be both a cure and eventual cause of symptoms. This does not mean that somebody should never have taken Parkinson's Disease drugs. Somebody should not also instantly cease their Parkinson's Disease drugs. They would get almost immediate withdrawal symptoms. It is just an unfortunate fact for drugs of many disorders that there are not only side effects, but an eventual opposite after effect that contributes to the medical disorder it initially relieved.
In this approach there is an attempt to find the cause and treat this using natural chelation therapies to attempt to remove the toxins and heavy metals. The observations provide more details here. Needless to say the sooner this is started the better. Brain damage cannot be reversed, but it can be halted in its spread.
The sequence of the symptoms I have shown need not be an inevitable consequence, it is possible to stop the spread at each stage as long as you work hard to find the cause. The other important aspect is to help your immune system fight the invaders. This is done by good food, laughter, friendship and company [love] , hobbies, fresh air and light exercise, communing with nature and so on - all the suppression actions.
- Eating for health is key DO NOT USE VITAMIN SUPLEMENTS OR MINERAL SUPPLEMENTS, you need to experience the sheer pleasure of eating fresh well balanced food, beautifully presented, and eaten slowly with friends and relatives. The emotional enjoyment you get from this is as healing as the food itself.
- Exercising and keeping fit - keeps the brain cells active and the body muscles from atrophying - they will relearn certain movements - the focus of activity will shift in the brain processors and in effect the constant relearning will keep you active
- Sleep as much as you can - Sleeping has a number of functions. One is the defragging of memory, another is learning from the perceptions gathered during the waking period, but the third purpose of sleep is healing.
Healing takes place during very deep non REM sleep, when the mind and body are totally inactive. This inactivity then gives the autonomic system and the healing processes a better chance to function. In some senses we go into a light coma every night when we fall asleep in a deep state of non dreaming sleep, but because we are never monitored in our own bed, no one knows.
Anyone who is being attacked by pathogens especially in the brain, needs a great deal of sleep, because it gives them the chance to relearn from perceptions and heal.
- Sun - one key vitamin often lacking in all western cultures is Vitamin D. It is possible to get Vitamin D from cod liver oil, but the ideal is to go out in the sun as often as you can. The ideal is actually to be naked in the sun, but as I am all too aware [the 'nipples like organ stops syndrome'] , this is not necessarily that practical in the northern countries. However, every little helps, so even an hour or so's exposure can make all the difference.
Additional therapies can also be used to help with stiffness etc if the disease has progressed to motor centres. Again the observations show where techniques such as osteopathy, physiotherapy, reiki, acupuncture, etc have helped. Manipulative and healing therapies can often be a great help because they help the body itself to relearn movements and keep it supple and flexible.
How it works
Why do some people get hallucinations, visions and even out of body experiences from Parkinson's disease? In very many instances, it appears to be the medication they are given - often in overdose proportions - that is the cause. But in those cases where it is not the medication, the mechanism is via the generic mechanism described under Brain damage.
References and further reading
I have provided a far more detailed description for some of the causes in Parkinson’s disease causes in detail.see also Neurologic adverse events following vaccination Prog Health Sci, 2012, Sienkiewicz D., Ku?ak W., Okurowska-Zawada B., Paszko-Patej G
- A review of the clinical evidence for complementary and alternative therapies in Parkinson's disease 012980
- Banana (Musa spp) from peel to pulp: ethnopharmacology, source of bioactive compounds and its relevance for human health 019294
- Cannabis and Parkinson's disease 012787
- CES and Parkinson's disease 006508
- Coffee and Parkinson's disease 005612
- Coffee, dopamine and addiction 005622
- Discovery of novel anti-parkinsonian effect of schisantherin A in in vitro and in vivo 020879
- Dr Duke's list of activity for Vitamin B6 017763
- Dr Duke's list of activity for Vitamin C 017762
- Dr Duke's list of biological activities for Vitamin C 017880
- Dr Duke's list of chemicals and activity for the Shallot 017969
- Dr Duke's list of Chemicals in Persea americana MILLER (Lauraceae) -- Avocado 012983
- Dr Duke's list of myorelaxant activity in Celery 012451
- Dr Duke's list of Plants with Antiataxic activity 018348
- Dr Duke's list of Plants with Antibradiquinic and Antibradykineticactivity 018355
- Dr Michael Thaut - Research with Parkinson's disease sufferers 021838
- Dr Natasha Campbell-McBride - The Gut and Psychology Syndrome (GAPS) Diet 027895
- Dr. Natasha Campbell-McBride - Heart attack through 'evil fats'? 027893
- Effects of Alexander Technique training experience on gait behavior in older adults 027449
- Escin, a novel triterpene, mitigates chronic MPTP/p-induced dopaminergic toxicity by attenuating mitochondrial dysfunction, oxidative stress, and apoptosis 019055
- Ficino, Marsilio - Commentary on Plato’s Timaeus - And music therapy 015985
- Gelder Kunz, Dora van - Predicting disease 004180
- Gupta, Robert – TEDtalk Between music and medicine - 02 021967
- Healing by AVOIDING all foods sprayed with glyphosate [Roundup] 026330
- Heavy metal poisoning and brain damage 006198
- How to Rid Your Body of Mercury and Other Heavy Metals: A 3-Step Plan to Recover Your Health 026662
- Irish set dancing and Parkinson's disease 013376
- Ketogenic diet in neuromuscular and neurodegenerative diseases 026609
- Mercury in foods and fish and selenium as a chelation agent 013083
- Metagenomic testing as a means of identifying the pathogens causing Parkinson's disease 026775
- Motor effects of broad beans (Vicia faba) in Parkinson's disease, single dose studies 022043
- Mrs Grieve on Mugwort [Artemisia vulgaris] 012749
- Neuroprotective effects of the cultivated Chondrus crispus in a C. elegans model of Parkinson's disease. 016973
- Nicotine and Parkinsons disease 005279
- Nicotine as Therapy 017963
- Nicotinic stimulation and Parkinson's disease 005278
- Oliver Sacks - Healing using music 022270
- Parkinson's disease and bananas 012982
- Parkinson's disease and cannabis 012981
- Parkinson's disease and chocolate 012978
- Parkinson's disease and cocaine 012979
- Parkinson's disease and dancing the tango 013368
- Parkinson's disease and manganese poisoning 006197
- Parkinson's disease forum - Reiki and massage 012976
- Standard osteopathic manipulative treatment acutely improves gait performance in patients with Parkinson's disease 012977
- Sulforaphane as a potential protective phytochemical against neurodegenerative diseases 021407
- Tai Chi for improvement of motor function, balance and gait in Parkinson's disease: a systematic review and meta-analysis 026380
- The healing effects of Vitamin D and sunlight 012466
- The Healing Power of Sleep 026790
- The Ketogenic Diet: Making a Comeback 026610
- The neuroprotective effects of purslane (Portulaca oleracea) on rotenone-induced biochemical changes and apoptosis in brain of rat 018908
- Apokyn 018004
- CNS Diseases and Uveitis 027568
- Common Drugs May Cause Cognitive Problems 021361
- Depression, drugs and nanoparticles 006339
- Dopamine agonist withdrawal syndrome: implications for patient care. 013025
- Effects and side effects associated with the non-nutritional use of tryptophan by humans 017320
- Elevated Serum Pesticide Levels and Risk of Parkinson Disease 027717
- Ergotism and pharmaceuticals 006805
- Exacerbation of Lewy bodies dementia due to memantine 012988
- Feelings of presence in Parkinson's disease 003442
- Flu and all its effects 006406
- Hallucinations and delusions 003444
- Hallucinations from welding the San Francisco Bridge 006900
- Hallucinations, brain damage and nanoparticles - Manufacturers and Cosmetic companies 006338
- Hitler, Adolf - cocaine and strychnine 001448
- John the bridge and the horse 006195
- Lateral geniculate atrophy in Parkinson's with visual hallucination: A trans-synaptic degeneration 027673
- Manganese and acute paranoid psychosis: a case report 013022
- Manganese poisoning 006816
- Manganese poisoning from mining, smelting and welding 001445
- Manganese poisoning from welding 001446
- Manganese poisoning from welding 006407
- Minor retinal degeneration in Parkinson's disease 019941
- Oliver Sacks - A 3D Taj Mahal 001522
- Oliver Sacks - L-DOPA, Parkinson's, Tourette's and mania 014344
- Parasitosis of the Central Nervous system 012791
- Parkinson's disease showing progressive conduction aphasia 026096
- Parkinsonism with multiple cysts in the bilateral striata 017809
- Parkinson’s disease and hypotension 001106
- Parlodel 015650
- Pathology of CNS parasitic infections 012792
- Pramipexole 015662
- Prevalence and phenomenology of olfactory hallucinations in Parkinson's disease 014727
- Progressive aphasia with Lewy bodies 026098
- Psychiatric disorders in neurology 020778
- Rivastigmine 015703
- Sublingual atropine for sialorrhea secondary to parkinsonism: a pilot study 019470
- Tactile hallucinations in patients with Parkinson's disease 014711
- The widening spectrum of C9ORF72-related disease; genotype/phenotype correlations and potential modifiers of clinical phenotype. 020775
- This Man’s Smell Hallucinations Can Predict the Weather 029549
- Visual hallucinations 003443
- Visual hallucinations and delirium during treatment with amantadine (Symmetrel) 023516
Wisdom, Inspiration, Divine love & Bliss
- Aluminum-induced entropy in biological systems: implications for neurological disease 015269
- Oliver Sacks - L-DOPA, Parkinson's, Tourette's and mania 014344
- Feelings of presence in Parkinson's disease 003442
- Gelder Kunz, Dora van - Predicting disease 004180
- Hallucinations and delusions 003444
- Manganese poisoning from mining, smelting and welding 001445
- Manganese poisoning from welding 001446
- Oliver Sacks - L-DOPA, Parkinson's, Tourette's and mania 014344
- Hack Tuke, Daniel – Sickness - Trembling Palsy, Paralysis Agitans, Parkinsons induced by powerful emotions – terror, insecurity, stress and anxiety 026080
- Metals and brain disease 006160
- Metals and Parkinson's Disease: Mechanisms and Biochemical Processes. 029499
- Nicotine patches in Alzheimer's disease: pilot study on learning, memory, and safety 027599
- Parkinson's disease and behavioural effects 006196
- Virus-like particles and enterovirus antigen found in the brainstem neurons of Parkinson's disease 027584