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10-26-2013, 11:32 AM | #31 | |||
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In Remembrance
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Thank you Mrs D. Yes, I had started the B-12 a couple of days earlier and was a bit reckless with it. I have no trouble believing the scenario. The strong reaction that I was getting was why I diluted it to such an exteme. It sounds as though I need to let it was out and approach more slowly on that.
I find your comment on the TSH to be very interesting and will follow up on it. Thanks. Quote:
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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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"Thanks for this!" says: | Conductor71 (10-27-2013) |
10-28-2013, 02:24 PM | #32 | |||
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In Remembrance
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Seminars in Neurology
Movement Disorders Caused by Medical Disease Brandon Barton, S. Elizabeth Zauber, Christopher G. Goetz Disclosures Semin Neurol. 2009;29(2):97-110. Abstract and Introduction Parkinsonism Nonparkinsonian Tremor Dystonia Chorea Future Perspectives References Related Articles The Differential Diagnosis of Huntington's Disease-like Syndromes Ultrasound Thalamotomy Benefits Essential Tremor Deep Brain Stimulation for Parkinson's Disease and Other Movement Disorders Parkinsonism The term parkinsonism describes a clinical syndrome with the cardinal motor features of rest tremor, rigidity, bradykinesia, and postural instability. Parkinsonism occurs due to disruption of the structure, physiology, or neurochemical function of the dopaminergic pathway traveling from the substantia nigra to the subcortical nuclei, including the putamen and caudate nucleus (striatum), thalami, and cortical circuits. This primary cell system can be influenced by involvement of the brainstem or other basal ganglia nuclei. Although the most common cause of parkinsonism is Parkinson's disease, a wide range of medical conditions and treatments may be associated with parkinsonian signs. Given that these secondary causes of parkinsonism may involve a different prognosis or treatment than Parkinson's disease, an individual patient presenting with parkinsonism requires a thorough medical history. In general, presentations of parkinsonism with rapid or subacute onset, mild or absent rest tremor, symmetric akinesia and rigidity, and early-onset gait disorder with postural instability suggest secondary causes of parkinsonism. Disorders of Metabolism Many kinds of metabolic disorders may cause parkinsonism. Thyroid Disease. Hypothyroidism shares many features in common with parkinsonism -- including rigidity, fatigue, masked facial expression, constipation, depression, and slowed movements, speech, and gait -- but can be distinguished from Parkinson's disease by other medical features and diagnostic studies of endocrine dysfunction. The development of hypothyroidism in the setting of Parkinson's disease may be mistaken for worsening parkinsonism, but the symptoms can improve with thyroid hormone replacement.[1] Conversely, hyperthyroidism may mimic the weight loss or increased sweating seen with Parkinson's disease or may exaggerate parkinsonian tremor, and improvement occurs with antithyroid treatment.[2] Renal Failure. Parkinsonism has been reported in patients with uremia due to end-stage renal disease, particularly in patients with concomitant diabetes.[3] Typical features include acute or subacute onset of parkinsonian symptoms and additional clinical features of altered consciousness, myoclonus, dysarthria, and ataxia. Neuroimaging findings include bilateral, symmetric, and reversible basal ganglia lesions with evidence of vasogenic edema.[4] Calcium Disorders. Disorders of calcium metabolism may occur in association with parkinsonism. Hypoparathyroidism has been reported to cause parkinsonism both in the presence and absence of basal ganglia calcifications. It may occur as a late complication after thyroidectomy[5] and may be responsive to levodopa in some cases
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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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"Thanks for this!" says: | Aunt Bean (10-30-2013) |
10-29-2013, 10:16 AM | #33 | ||
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Senior Member
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Quote:
We have yet to do the 24-hour calcium test, but that's on the list. There is a group in Florida that specializes in the parathyroid, I would google them if you even remotely think you may have an issue with that gland: the symptoms are almost identical to PD. They even have an app you can buy to see the likelihood of having an issue, but you must have had the thyroid tests and calcium tests done first so you can input the data. the good news: if you have an issue with your parathyroid, these guys do a surgery that can cure it, it's amazing. |
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"Thanks for this!" says: | Aunt Bean (10-30-2013), Conductor71 (11-04-2013) |
11-12-2013, 03:28 PM | #34 | |||
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Member
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Just got back from doctor's appointment . Asked about magnesium citrate. She said it was not harmful in small doses, but would prefer I would use milk of magnesia . For some reason, I am absolutely sure magnesium citrate has a definite bearing on my PD symptoms. My bowels are finally moving practically normally ...taking 2 teas of CALM a day. Finished it yesterday and am ready to start a less expensive container from Swansons to see how it does, and if it is as efficient as the other. It is crazy not to have my PD symptoms without taking much tincture. TWO possibilities...
1. constipation was from way back in 7th grade after my diving accident, when I first started the right leg drag and foot turn also. Constipation creates toxins... just having that out of the way could help reduce symptoms 2. magnesium citrate has some bearing on how the l-dopa is used or stored or on how the neurons function. Any thoughts out there ???? Anyway, I am very impressed with the results taking a low dose of it daily so far and hope this remains an ongoing (excuse the pun) occurrence . It will mean having to make and use less tincture (a savings on my back as far as field work). And, I feel so good! |
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"Thanks for this!" says: | Stand Tall (11-13-2013) |
11-27-2013, 08:29 AM | #35 | |||
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I have found that" Natural Calm " product is more effective than just plain magnesium citrate for some reason (as far as helping the bowels and making l-dopa last longer)...not sure what is extra in this product (it fizzes and a plain supplement I purchased doesn't))... need to contact the company and find out.
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