[imark3000]

It struck me that the above topic is not discussed on this forum. There are plenty of research which suggest to me that subtypes of PD originate in damage of different areas in the brain (below link is an example). The sub types need in my opinion different strategies of treatment and drugs but neurologists don't seem to recognise this and have only one course of treatment fo all. What do you think?

Imad

http://journals.lww.com/co-neurology...nsonism.9.aspx
AbstractPurpose of review: Akinesia, rigidity and low-frequency rest tremor are the three cardinal motor signs of Parkinson's disease and some Parkinson's disease animal models. However, cumulative evidence supports the view that akinesia/rigidity vs. tremor reflect different pathophysiological phenomena in the basal ganglia. Here, we review the recent physiological literature correlating abnormal neural activity in the basal ganglia with Parkinson's disease clinical symptoms.

Recent findings: The subthalamic nucleus of Parkinson's disease patients is characterized by oscillatory activity in the beta-frequency (∼15 Hz) range. However, Parkinson's disease tremor is not strictly correlated with the abnormal synchronous oscillations of the basal ganglia. On the other hand, akinesia and rigidity are better correlated with the basal ganglia beta oscillations.

Summary: The abnormal basal ganglia output leads to akinesia and rigidity. Parkinson's disease tremor most likely evolves as a downstream compensatory mechanism.

[imark3000]

http://www.molecularstation.com/rese...-18098275.html

Tremor dominant parkinsonism (TDP) is characterized by initial prominent resting and action tremor, mild parkinsonism, unpredictable response to medication, and a better prognosis than idiopathic Parkinson's disease (PD). We report on clinical features and longitudinal course of 26 patients suffering from TDP. Mean disease duration was 6.5 +/- 3 years, 61.5% of patients had a positive family history of tremor, 73% did not need drug treatment, performance of 123I-Ioflupane SPECT showed reduced striatal tracer uptake in 65.4% of patients, and odor identification testing was pathologic in all the patients tested (n = 22). Co-occurrence of action and resting tremor were the most annoying and disabling symptoms in all the patients, whereas rigidity and/or bradykinesia were clinically irrelevant in most of them. We also sequenced the full coding region of the Leucine-rich repeat kinase 2 gene (LRRK2) in all patients. We found a novel Val2390Met mutation that was not found in 864 chromosomes. Our results suggest a broader clinical heterogeneity related to LRRK2 mutations and points towards TDP as a subtype within the spectrum of PD, in which disabling tremor but otherwise mild parkinsonian signs and a better prognosis are the main characteristics. (c) 2007 Movement Disorder Society.
Imad

[imark3000]

Defining PD Subtypes Based on Patterns of Long-term Outcome
PD Subtypes 2007

http://www.michaeljfox.org/research_...s_3.cfm?ID=303



The purpose of our study is to identify Parkinson’s disease subtypes based on how individuals are doing approximately seven to eight years after diagnosis. Some patients have few symptoms at this time, while others may have problems with thinking and memory, balance, mood, motor fluctuations and dyskinesia, parkinsonism (slowness, stiffness, tremor), or autonomic function (blood pressure, urinary, and bowel function). We will analyze two long-term studies (DATATOP - Deprenyl and Tocopherol Antioxidant Therapy of Parkinsonism and CALM-PD - Comparison of the Agonist Pramipexole with Levodopa on Motor Complications of Parkinson’s Disease) and attempt to identify groups of patients with similar patterns of symptoms. We will then analyze characteristics of these patients when they were first diagnosed and treated to determine if we are able to predict their pattern of symptoms seven to eight years after diagnosis.



Early identification of patients who are anticipated to develop particular patterns of symptoms may allow selection of specific therapies that will improve long-term outcome and specific subtypes of patients may be selected for entry into clinical trials designed to evaluate therapies to forestall the development of that pattern of symptoms. In addition, identification of distinct PD subtypes may aid in delineating genetic and environmental causes of PD

[imark3000]

http://www.pdonlineresearch.org/resp...difficulty-pig

[Sasha]

thanks - this makes so much sense to me - I am definitely the rigid type - since I don't have a tremor (except when anxious, way too often) people often think I don't have Parkinson's or have a very mild case - when In fact I'm medicated to the gills just to walk across the floor! Muscle relaxants help. I also have a tendency to joint problems, bursitis, tendinitis, etc. which I think is all related. Anyone else?

[Sasha]

Is there some way to look up these articles as opposed to only the abstract? I would like to wade into the article a bit....

Thanks.

[Conductor71]

Hey,

Just wanted to add that we do definitely discuss this one. There was a recent one started last month, I think, (by me) and in searching the archives there are discussions going back a few years.

http://neurotalk.psychcentral.com/sh...light=subtypes

http://neurotalk.psychcentral.com/sh...light=subtypes

This is very important to our lives because these subtypes most likely explain why we have different symptoms and have varying reactions to meds. It may factor in diagnostic issues at the clinical level, and at the research level may impact clinical trial outcomes in the search for new therapies.

Recently, MJFF posed a question on PDOnline Research inviting researchers to share what direction or questions might be asked regarding subtypes. I'm not sure that there has been much of a response.

Laura

[imark3000]

Laura: Sorry for my forgetfullness ! as the topic was indeed raised and discussed before on this forum and thank you for providing the links

Sasha: Great to know that you are willing and able to dig deep into research while I get mentally tiered if I try to go beyond scratching the surface ! and this is definitly due to my pd as I had much more patience and mental vigour befeore. As to your question, I think that you need to subscribe if you need the full text.

thanks to all .

Imad

[ZucchiniFlower]

Hi, I've discussed this over the years. Even my conversations about closed and open loops, and the benefit of external cues, is related.

I'm disappointed the most here don't seem to want to try auditory, visual, imaginary cues to improve their condition. Without them, I'm a basket case. Whenever I made a specific suggestion, no one tried it. Some do try an expensive device that does the same thing.

Thinking "side to side", as if rocking in my brain, instead of thinking about moving forward helps me resolve bradykinesia and akinesia. I exit the train much faster with imaginary cues. I also use visual cues at the same time, usually lines on the sidewalk, or leaves, or my imagination again.

Internal metronome helps enormously. Singing, counting, using my cane, do too.

I believe the cues reinforce new loops, discussed in this OLD article:

interactive report THEY LIKE FEEDBACK FROM OTHERS, TOO!

Basal ganglia and cerebellar loops: motor and cognitive circuits


Frank A. Middletona and Peter L. Stricka, b, c, *

a Research Service (151S), VA Medical Center, 800 Irving Ave., Syracuse, NY 13210, USA

b Department of Neurosurgery, State University of New York Health Science Center at Syracuse, Syracuse, NY USA

c Department of Neuroscience/Physiology, State University of New York Health Science Center at Syracuse, Syracuse, NY USA

Accepted 30 June 1999.
Available online 13 March 2000.

Abstract

The traditional view that the basal ganglia and cerebellum are simply involved in the control of movement has been challenged in recent years. One of the pivotal reasons for this reappraisal has been new information about basal ganglia and cerebellar connections with the cerebral cortex. In essence, recent anatomical studies have revealed that these connections are organized into discrete circuits or ‘loops'. Rather than serving as a means for widespread cortical areas to gain access to the motor system, these loops reciprocally interconnect a large and diverse set of cerebral cortical areas with the basal ganglia and cerebellum.

The properties of neurons within the basal ganglia or cerebellar components of these circuits resembles the properties of neurons within the cortical areas subserved by these loops. For example, neuronal activity within basal ganglia and cerebellar loops with motor areas of the cerebral cortex is highly correlated with parameters of movement, while neuronal activity within basal ganglia and cerebellar loops with areas of the prefrontal cortex is more related to aspects of cognitive function.

Thus, individual loops appear to be involved in distinct behavioral functions. Studies of basal ganglia and cerebellar pathology support this conclusion. Damage to the basal ganglia or cerebellar components of circuits with motor areas of cortex leads to motor symptoms, whereas damage of the subcortical components of circuits with non-motor areas of cortex causes higher-order deficits.

In this report, we review some of the new anatomical, physiological and behavioral findings that have contributed to a reappraisal of function concerning the basal ganglia and cerebellar loops with the cerebral cortex.

http://www.sciencedirect.com/science...b37fc5ad1b8210