Parkinson's Disease Tulip


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Old 07-24-2010, 03:08 PM #1
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Default Dyskinesia

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
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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 07-24-2010, 03:48 PM #2
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Default Dextromethorphan for dyskinesia

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.
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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 07-24-2010, 03:53 PM #3
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Default Mucuna pruriens for dyskinesia

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.
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Old 07-24-2010, 03:59 PM #4
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Default Creatine and dyskinesia

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.
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Old 07-24-2010, 04:03 PM #5
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Default Vitamin B6

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.
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Old 07-24-2010, 04:06 PM #6
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Default Quercetin

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.
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Old 07-24-2010, 04:11 PM #7
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Default Melatonin

1. Arch Gen Psychiatry. 2001 Nov;58(11):1049-52.

Melatonin treatment for tardive dyskinesia: a double-blind, placebo-controlled,
crossover study.

Shamir E, Barak Y, Shalman I, Laudon M, Zisapel N, Tarrasch R, Elizur A, Weizman
R.

Abarbanel Mental Health Center, 15 KKL St, Bat-Yam 59100, Israel.
drshamir@hotmail.com

Comment in:
Arch Gen Psychiatry. 2001 Nov;58(11):1054-5.

BACKGROUND: Antipsychotics remain the mainstay of drug intervention in the
management of schizophrenia. However, long-term treatment with antipsychotics is
associated with a variety of movement disorders, the most disabling of which is
tardive dyskinesia (TD), which occurs in up to 50% of patients hospitalized with
chronic schizophrenia. The pathophysiology of TD is still unclear and no definite
treatment exists. Both dopamine receptor supersensitivity and oxidative
stress-induced neurotoxicity in the nigrostriatal system are apparently
implicated. The pineal hormone melatonin is a potent antioxidant and attenuates
dopaminergic activity in the striatum and dopamine release from the hypothalamus.
Thus, it may have a beneficial effect for both the treatment and prevention of
TD. METHODS: Using a double-blind, placebo-controlled, crossover study, we
evaluated the efficacy of 10 mg/d of melatonin for 6 weeks in 22 patients with
schizophrenia and TD. The primary outcome measure was the change from baseline in
Abnormal Involuntary Movement Scale (AIMS) score. RESULTS: The decrease (mean +/-
SD) in AIMS score was 2.45 +/- 1.92 for the melatonin and 0.77 +/- 1.11 for the
placebo treatment groups (P<.001). No adverse events or side effects were noted.
CONCLUSION: This is the first clinical evidence for efficacy of melatonin in the
treatment of TD.

PMID: 11695951 [PubMed - indexed for MEDLINE]
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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 07-24-2010, 05:31 PM #8
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Default

6:20 Dk down to 25% level. Feel no need for meds.
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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 07-25-2010, 01:58 AM #9
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Default Dyskinesia,

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
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Old 07-25-2010, 03:56 AM #10
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Ron,
Just a thought, have you changed the way your l-dopa is delivered?

Lindy
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