FAQ/Help |
Calendar |
Search |
Today's Posts |
|
07-24-2010, 03:08 PM | #1 | |||
|
||||
In Remembrance
|
Ron-
I've been scratching around for a couple of hours and found nothing to make me wonder about either curcumin or citicholine. Research is sparse, but I did find a promising few old friends and I'll list them individually. -Rick
__________________
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. |
|||
Reply With Quote |
"Thanks for this!" says: | Soozie (07-24-2010) |
07-24-2010, 03:48 PM | #2 | |||
|
||||
In Remembrance
|
In true white rat fashion, I am testing this one even as we type. It is presently 4:18 PM here and I've been dyskinetic for the last couple of hours and expect to be so for a couple more. So, I took a quarter teaspoon at 4:15 and will report later.
1. Mov Disord. 1998 May;13(3):414-7. A trial of dextromethorphan in parkinsonian patients with motor response complications. Verhagen Metman L, Blanchet PJ, van den Munckhof P, Del Dotto P, Natté R, Chase TN. Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1406, USA. The effects of the NMDA antagonist dextromethorphan (DM) on levodopa-associated dyskinesias and motor fluctuations were studied in patients with advanced Parkinson's disease. During initial open-label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60-120 mg/day). The 12 remaining patients either experienced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double-blind, placebo-controlled, crossover study with two 2-week arms separated by 1 week wash-out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% according to UPDRS interviews, without compromising the anti-Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. Although the narrow therapeutic index of DM limits its clinical usefulness, these findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate levodopa-associated motor complications. PMID: 9613730 [PubMed - indexed for MEDLINE] 1. Amino Acids. 1998;14(1-3):75-82. Blockade of glutamatergic transmission as treatment for dyskinesias and motor fluctuations in Parkinson's disease. Verhagen Metman L, Del Dotto P, Blanchet PJ, van den Munckhof P, Chase TN. National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, USA. In animal models of Parkinson's disease (PD), glutamate antagonists diminish levodopa (LD)-associated motor fluctuations and dyskinesias. We sought to investigate if these preclinical observations can be extended to the human disease, by evaluating the effects of three non-competitive NMDA antagonists (dextrorphan, dextromethorphan and amantadine) on the motor response to LD in patients with advanced PD. In four separate trials, adjuvant therapy with these drugs reduced LD-induced dyskinesias and motor fluctuations. These findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate LD associated motor response complications. PMID: 9871445 [PubMed - indexed for MEDLINE] 1. Neurology. 1998 Jul;51(1):203-6. Dextromethorphan improves levodopa-induced dyskinesias in Parkinson's disease. Verhagen Metman L, Del Dotto P, Natté R, van den Munckhof P, Chase TN. Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892-1406, USA. OBJECTIVE: This study assessed the effects of the N-methyl-D-aspartate (NMDA) antagonist dextromethorphan (DM) on levodopa-induced dyskinesias in Parkinson's disease (PD). BACKGROUND: Recent experimental evidence suggests that increased synaptic efficacy of NMDA receptors expressed on basal ganglia neurons may play a role in the pathophysiology of levodopa-induced motor response complications. METHODS: DM was given to six PD patients with motor fluctuations in a double-blind, placebo-controlled, cross-over study. At the end of each 3-week study arm, patients received several brief i.v. levodopa infusions while parkinsonian symptoms and dyskinesias were frequently scored. Levodopa dose-response curves for antiparkinsonian and dyskinetic effects were then compared for each study arm. RESULTS: With DM, average and maximum dyskinesia scores improved by >50%, without compromising the antiparkinsonian response magnitude or duration of levodopa, although in some subjects the levodopa threshold dose was slightly higher with DM than with placebo. CONCLUSIONS: These findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptors can ameliorate levodopa-associated dyskinesias. PMID: 9674803 [PubMed - indexed for MEDLINE] Remember a couple of things about dextromethorphan- 1- Less is more. Take the least dose that gives you the effect as a little more will reverse the effect. 2- When you do your research, be aware that dextromethorphan gives the Drug Warriors apoplexy because it is so readily available and has so few side effects. So they put out a lot of lies about it. BTW, it is now 4:41 PM and my dk is down by a third.
__________________
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. |
|||
Reply With Quote |
07-24-2010, 03:53 PM | #3 | |||
|
||||
In Remembrance
|
Some recent work
1. Nat Prod Res. 2010 Jul 13:1-8. [Epub ahead of print] Mucuna pruriens attenuates haloperidol-induced orofacial dyskinesia in rats. Pathan AA, Mohan M, Kasture AS, Kasture SB. Department of Pharmacology, MGV's Pharmacy College, Panchavati, Nashik, Maharashtra, India. Neuroleptic-induced tardive dyskinesia (TD) is a motor disorder of the orofacial region resulting from chronic neuroleptic treatment. The agents improving dopaminergic transmission improve TD. Mucuna pruriens seed contains levodopa and amino acids. The effect of methanolic extract of M. pruriens seeds (MEMP) was studied on haloperidol-induced TD, alongside the changes in lipid peroxidation, reduced glutathione, superoxide dismutase (SOD) and catalase levels. The effect of MEMP was also evaluated in terms of the generation of hydroxyl and 1,1-diphenyl,2-picrylhydrazyl (DPPH) radical. MEMP (100 and 200 mg kg(-1)) inhibited haloperidol-induced vacuous chewing movements, orofacial bursts and biochemical changes. MEMP also inhibited hydroxyl radical generation and DPPH. The results of the present study suggest that MEMP by virtue of its free radical scavenging activity prevents neuroleptic-induced TD. PMID: 20635303 [PubMed - as supplied by publisher]
__________________
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. |
|||
Reply With Quote |
07-24-2010, 03:59 PM | #4 | |||
|
||||
In Remembrance
|
Creatine is the "Poor Man's CoQ10 and is in trials somewhere. It is widely used in the sports world-
1. Behav Brain Res. 2009 Jan 30;197(1):90-6. Epub 2008 Aug 12. Oral creatine supplementation attenuates L-DOPA-induced dyskinesia in 6-hydroxydopamine-lesioned rats. Valastro B, Dekundy A, Danysz W, Quack G. Preclinical Research and Development, In Vitro Screening, Merz Pharmaceuticals GmbH, Altenhöferallee 3, 60438 Frankfurt am Main, Germany. L-DOPA-induced dyskinesia (LID) is among the motor complications that arise in Parkinson patients after a prolonged treatment with levodopa (L-DOPA). Since previous transcriptome and proteomic studies performed in the rat model of LID suggested important changes in striatal energy-related components, we hypothesize that oral creatine supplementation could prevent or attenuate the occurrence of LID. In this study, 6-hydroxydopamine-lesioned rats received a 2% creatine-supplemented diet for 1 month prior to L-DOPA therapy. During the 21 days of L-DOPA treatment, significant reductions in abnormal involuntary movements (AIMs) have been observed in the creatine-supplemented group, without any worsening of parkinsonism. In situ hybridization histochemistry and immunohistochemistry analysis of the striatum also showed a reduction in the levels of prodynorphin mRNA and FosB/DeltaFosB-immunopositive cells in creatine-supplemented diet group, an effect that was dependant on the development of AIMs. Further investigation of the bioenergetics' status of the denervated striatum revealed significant changes in the levels of creatine both after L-DOPA alone and with the supplemented diet. In conclusion, we demonstrated that combining L-DOPA therapy with a diet enriched in creatine could attenuate LID, which may represent a new way to control the motor complications associated with L-DOPA therapy. PMID: 18762218 [PubMed - indexed for MEDLINE]
__________________
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. |
|||
Reply With Quote |
07-24-2010, 04:03 PM | #5 | |||
|
||||
In Remembrance
|
1. J Clin Psychiatry. 2007 Nov;68(11):1648-54.
Vitamin B6 treatment for tardive dyskinesia: a randomized, double-blind, placebo-controlled, crossover study. Lerner V, Miodownik C, Kaptsan A, Bersudsky Y, Libov I, Sela BA, Witztum E. Division of Psychiatry, Ministry of Health Be'er Sheva Mental Health Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Be'er-Sheva, Israel. lernervld@yahoo.com BACKGROUND: Tardive dyskinesia (TD) is a significant clinical problem. Vitamin B(6) is a potent antioxidant and takes part in almost all of the possible mechanisms that are suggested as being associated with appearance of TD. The aims of this study were (1) to reexamine the efficacy and safety of higher doses of vitamin B(6) versus placebo in a greater sample of patients for a longer time and (2) to evaluate the carryover effect of vitamin B(6). METHOD: A 26-week, double-blind, placebo-controlled trial was conducted in a university-based research clinic from August 2002 to January 2005 on 50 inpatients with DSM-IV diagnoses of schizophrenia or schizoaffective disorder and TD. In a double-blind crossover paradigm, all study subjects were randomly assigned to start treatment with either vitamin B(6) (daily dose of 1200 mg) or placebo. After 12 weeks of treatment and then a 2-week washout, subjects were crossed over to receive the other treatment for 12 weeks. The primary outcome measure was the change from baseline in Extra-pyramidal Symptom Rating Scale (ESRS) scores. RESULTS: The mean decrease in ESRS clinical global impression scores from baseline to endpoint was 2.4 points in patients treated with vitamin B(6) and 0.2 points in patients treated with placebo (p < .0001). The mean decrease in the parkinsonism subscale score was 18.5 points and 1.4 points, respectively (p < .00001), and the mean decrease in the dyskinesia subscale score was 5.2 points and -0.8 points, respectively (p < .0001). CONCLUSION: Vitamin B(6) appears to be effective in reducing symptoms of TD. The specific mechanisms by which vitamin B(6) attenuates symptoms of TD are not clear. PMID: 18052557 [PubMed - indexed for MEDLINE]
__________________
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. |
|||
Reply With Quote |
07-24-2010, 04:06 PM | #6 | |||
|
||||
In Remembrance
|
1. Neuropharmacology. 2003 Jun;44(8):1100-6.
Quercetin, a bioflavonoid, attenuates haloperidol-induced orofacial dyskinesia. Naidu PS, Singh A, Kulkarni SK. Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, -160014, Chandigarh, India. Chronic treatment with neuroleptics leads to the development of abnormal orofacial movements described as vacuous chewing movements (VCMs) in rats. Vacuous chewing movements in rodents are widely accepted as one of the animal models of tardive dyskinesia. Oxidative stress and the products of lipid peroxidation are implicated in the pathophysiology of various neurological disorders including tardive dyskinesia. In the present study chronic haloperidol (1.0 mg kg(-1) for 21 days) treatment induced vacuous chewing movements and tongue protrusions in rats. Co-administration of quercetin, a bioflavonoid, dose dependently (25-100 mg kg(-1)) reduced haloperidol-induced vacuous chewing movements and tongue protrusions. Biochemical analysis revealed that chronic haloperidol treatment induces lipid peroxidation and decreases the glutathione (GSH) levels in the forebrains of rats. The antioxidant defense enzymes, superoxide dismutase (SOD) and catalase were also decreased due to chronic haloperidol treatment. Co-administration of quercetin (25-100 mg kg(-1)) significantly reduced the lipid peroxidation and restored the decreased glutathione levels in these animals. Further quercetin (50-100 mg kg(-1)) also reversed the haloperidol-induced decrease in forebrain SOD and catalase levels in rats. The major findings of the present study suggested that oxidative stress plays a significant role in neuroleptic-induced orofacial dyskinesia and quercetin co-administration reverses these behavioral and biochemical changes. Quercetin, a naturally occurring bioflavonoid could prove to be a useful agent in neuroleptic-induced orofacial dyskinesia. PMID: 12763102 [PubMed - indexed for MEDLINE]
__________________
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. |
|||
Reply With Quote |
07-24-2010, 05:31 PM | #7 | |||
|
||||
In Remembrance
|
6:20 Dk down to 25% level. Feel no need for meds.
__________________
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. |
|||
Reply With Quote |
07-25-2010, 01:58 AM | #8 | |||
|
||||
In Remembrance
|
Rick,
I take my hat off to you, that is an incredible amount of work. These days, I just never seem to have the time. However I am still doing a lot of work for Kings College Hospital London, literature searches, fundraising etc. Looking at the prescription drugs for dyskinesia, amantadine is effective , but looses its effectiveness after around 6 months of use. It is an antiviral drug, and a very similar drug is Rimantadine, with a similar structure. Yesterday, I went to a Christening, and took half a 50mg Stavelo (25mg L-dopa) at 12-30pm. I writhed with dyskinesia until nearly 4-00pm. I can't take less than 25mg L-dopa!! Some time ago, there was no way 50mg would switch me on. It must mean my threshold level of sensitivity to L-dopa has reduced. Is it caused by prolonged use of curcumin, (it repairs BBB), and will I eventually not need L-dopa? Ron
__________________
Diagnosed Nov 1991. Born 1936 |
|||
Reply With Quote |
07-25-2010, 03:56 AM | #9 | ||
|
|||
Senior Member
|
Ron,
Just a thought, have you changed the way your l-dopa is delivered? Lindy |
||
Reply With Quote |
07-25-2010, 06:34 AM | #10 | |||
|
||||
In Remembrance
|
Quote:
I had tried Stavelo before, but did not like the lack of control over the amount of entacapone I was getting. If I rememer correctly, entacapone has a reputation for increasing dyskinesia I fly to Scotland for a week, at the end of next week, so I won't be able to keep posting. Ron
__________________
Diagnosed Nov 1991. Born 1936 |
|||
Reply With Quote |
Reply |
|
|
Similar Threads | ||||
Thread | Forum | |||
DXM really does stop dyskinesia | Parkinson's Disease | |||
Dyskinesia Question | Parkinson's Disease | |||
Dextromethorphan for dyskinesia? | Parkinson's Disease | |||
Dyskinesia Debut? | Parkinson's Disease | |||
Mucuna and dyskinesia | Parkinson's Disease |