Parkinson's Disease Tulip

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Old 12-12-2008, 03:50 PM #1
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Default Beans, Roots, and Leaves: History of PD Treatments

http://www.opus-bayern.de/uni-wuerzb...opus=122&la=de

This is a HUGE book on the history of PD and it is easy to read and it is free. Among the things you will find:
There have been a lot of other treatments before L-dopa and some seem to have worked as well.
Symptoms have changed considerably over the last 200 years.
Salvation has been just around the corner for an uncomfortably long time.
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 12-12-2008, 03:57 PM #2
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times until the near present (1980). It is not clear whether parkinsonism as it is now defined – a progressive neurodegenerative disorder of the basal ganglia characterized by sharply reduced striatal dopamine levels, particularly in the striatum – has always affected a significant minority of aged persons, but suggestive evidence to this effect in the older literature is reviewed. The major discussion commences, however, with the administration of various plant alkaloids to parkinsonian patients in the second half of the 19th century. Antiparkinsonian therapy since this time may be divided into a number of phases: 1. The employment of alkaloids derived from solanaceous plants: initially hyoscyamine, then hyoscine/scopolamine and atropine. The discovery and characterization of these alkaloids, and the gradual recognition that other pharmacologically useful solanaceous alkaloids (such as duboisine) were identical with one or other of these three compounds, is discussed. 2. With the outbreak of encephalitis lethargica following the First World War, parkinsonian patient numbers increased dramatically, leading to a multiplicity of new directions, including the use of another solanaceous plant, stramonium, of extremely high atropine doses, and of harmala alkaloids. 3. The so-called “Bulgarian treatment” was popularized in western Europe in the mid-1930s. It was also a belladonna alkaloid-based therapy, but associated with greater efficacy and fewer side effects. This approach, whether as actual plant extracts or as defined combinations of belladonna alkaloids, remained internationally dominant until the end of the 1940s. 4. Synthetic antiparkinsonian agents were examined following the Second World War, with the aim of overcoming the deficiencies of belladonna alkaloid therapy. These agents fell into two major classes: synthetic anticholinergic (= antimuscarinic) agents, such as benzhexol, and antihistaminergic drugs, including diphenhydramine. These agents were regarded as more effective than plant-based remedies, but certainly not as cures for the disease. 5. A complete change in direction was heralded by the discovery in 1960 of the striatal dopamine deficit in parkinsonism. This led to the introduction of L-DOPA therapy for parkinsonism, the first approach directed against an identified physiological abnormality in the disorder. 6. Subsequent developments have thus far concentrated on refinement or supplementation of the L-DOPA effect. Recent attempts to develop neuroprotective or -restorative approaches are also briefly discussed. The thesis also discusses the mechanisms by which the various types of antiparkinsonian agent achieved their effects, and also the problems confronting workers at various periods in the design and assessment of novel agents. The impact of attitudes regarding the etiology and nature of parkinsonism, particularly with regard to symptomatology, is also considered. Finally, the history of antiparkinsonian therapy is discussed in context of the general development of both clinical neurology and fundamental anatomical, physiological and biochemical research. In particular, the deepening understanding of the neurochemical basis of central nervous system function is emphasized, for which reason the history of dopamine research is discussed in some detail. This history of antiparkinsonian therapy also illustrates the fact that the nature of experimental clinical pharmacology has markedly changed throughout this period: No longer the preserve of individual physicians, it is now based firmly on fundamental laboratory research, the clinical relevance of which is not always immediately apparent, and which is only later examined in (large scale) clinical trials. It is concluded that antiparkinsonian therapy was never irrational or without basis, but has always been necessarily rooted in current knowledge regarding neural and muscular function. The achievements of L-DOPA therapy, the first successful pharmacological treatment for a neurodegenerative disorder, derived from the fruitful union of the skills and contributions of different types by laboratory scientists, pharmacologists and clinicians
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 10-08-2009, 08:06 PM #3
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Default bump for aunt bean

bump bump bump
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 10-08-2009, 08:40 PM #4
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What does bump mean? I can't believe I found your post again after looking from pg 1 to 58 last night for it! Thanks for the info
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Old 10-09-2009, 05:19 AM #5
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I think the main problem for a PD treatment is the poor knowledge of brain chemistry, the interactions among its different parts and the whole brain-body interaction.

My understanding is that current treatments are mostly focused on the lack of dopamine, and there's a need to target the other uncontrolled chemicals in our brains: glutamate, GABA, Fe, Ca, alpha-synuclein.

But my hope is that scientists will indeed find a way to stop PD. They have now much more powerful tools to research and, though it might seem a little rude, there's big business for those who find the cure (and that is a powerful incentive in today's business world).
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Old 05-22-2015, 09:44 AM #6
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Quote:
Originally Posted by reverett123 View Post
http://www.opus-bayern.de/uni-wuerzb...opus=122&la=de

This is a HUGE book on the history of PD and it is easy to read and it is free. Among the things you will find:
There have been a lot of other treatments before L-dopa and some seem to have worked as well.
Symptoms have changed considerably over the last 200 years.
Salvation has been just around the corner for an uncomfortably long time.
Thanks for this!! I love this stuff! I remain convinced that today's researcher/clinicians are on the wrong path too, and i think that a lot of modern pharmaceuticals make the disease worse - i.e. Citalopram (which i got stuck on to help me wean of clonazepam) the product monograph cites side effects that are a LOT like Parkinsonism....Ashford, in her withdrawal manual for benzodiazepines states that 3 of her patients got diagnosed by neurologists as having MS. Anyway, this is great reading.
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