Early cortical pacemaker improves Parkinson’s QoL

Photo Credits: CargoCollective

Parkinson’s disease is currently treated by dopamine agonists followed by deep brain stimulation later in the progression of the disease. However, A group of European researchers suggest deep brain stimulation via brain pacemaker earlier than currently used can improve the quality of life of patients with parkinson’s disease.

Parkinson’s is a neurodegenerative disease that affects mostly those in the upper age of life (> 50 years old), but can affect those as young as 20 if passed through genetics. As less and less dopamine is released by nerves in the brain, chemical messages become weaker and/or non-existent to the point of muscle movement becoming jerky, slow, and rigid. Unwanted shaking deemed ‘tremors’ also may develop. Current treatment is levadopa (a dopamine precursor) or dopamine agonist supplementation followed by (later in the disease) deep brain stimulation (subthalamic nucleus). This is meant to directly stimulate the nerves that are not receiving dopamine as they should.

To test if earlier stimulation than normally initiated could improve parkinson’s patients’ quality of life, a trial with 251 participants with early motor complications who either received normal medical treatment and early neurostimulation or solely normal medical treatment was conducted. The trial lasted two years with patient age averaging 52.

Using the 39 point Parkinson’s Disease Questionnaire, an improvement of 7.8 (average) points was seen in those getting the early stimulation treatment. Those not receiving the early neurostimulation showed an average decrease of 0.2 points at two years (P = 0.002).

The investigation group also showed greater improvement in motor disability (16.4 pt. difference, P <0.001), activities of daily living (6.2 pt. difference, P < 0.001), levodopa-induced motor complications (4.1 pt. difference, P < 0.001), and time without dyskinesia (1.9 hours more, P = 0.01).

Overall the group receiving the early cortical pacemaker for deep brain stimulation showed improvements in their quality of life compared to the group receiving standard medical treatment. Regarding safety however, 17.7% of those with implants had serious adverse events including nonspecific edema. Perhaps these are the risks of the surgery no matter if it comes early on or later in the progression.

This study suggests that deep brain stimulation can be used earlier in the disease progression to significantly improve the quality of life in those with parkinson’s disease.

Reference:
W.M.M. Schuepbach, J. Rau, K. Knudsen, J. Volkmann, P. Krack, L. Timmermann, T.D. Hälbig, H. Hesekamp, S.M. Navarro, N. Meier, D. Falk, M. Mehdorn, S. Paschen, M. Maarouf, M.T. Barbe, G.R. Fink, A. Kupsch, D. Gruber, G.-H. Schneider, E. Seigneuret, A. Kistner, P. Chaynes, F. Ory-Magne, C. Brefel Courbon, J. Vesper, A. Schnitzler, L. Wojtecki, J.-L. Houeto, B. Bataille, D. Maltête, P. Damier, S. Raoul, F. Sixel-Doering, D. Hellwig, A. Gharabaghi, R. Krüger, M.O. Pinsker, F. Amtage, J.-M. Régis, T. Witjas, S. Thobois, P. Mertens, M. Kloss, A. Hartmann, W.H. Oertel, B. Post, H. Speelman, Y. Agid, C. Schade-Brittinger, and G. Deuschl. Neurostimulation for Parkinson’s Disease with Early Motor Complications. The New England Journal of Medicine, 2013.
http://dx.doi.org/10.1056/NEJMoa1205158

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Dopamine copy-cat to treat Parkinson’s mimic

Dopamine

A Saudi Arabian family was found to have a genetic mutation leading to symptoms similar to parkinson’s disease, but the normal tests for the disease indicated otherwise. Researchers of the University of Toronto found that using a dopamine agonist reversed this parkinsonian condition almost completely.

Of this family, eight children, with a 16 year old as the eldest, were found to have symptoms of brain dopamine-serotonin vesicular transport disease, a VMAT2 deficiency. VMAT2 is a transporter protein that escorts dopamine across the neuronal synapse to its receptor.

Dopamine, in this context, serves as a way for neurons to communicate signals to each other. This was the mechanism breaking down in these children. The children’s symptoms from not having this neurotransmitter transporter were slow walking, difficulty initiating movement, droopy eyelids, audible breathing, dystonia, and other dopamine deficiency signs.

Through analysis of single nucleotide polymorphisms (SNPs pronounces “snips”) a mutation of the SLC18A2 gene was found as the cause of the VMAT2 absence.

To treat, the children were given a compound that activates dopamine receptors, a dopamine agonist, in hopes of making up for the neurotransmitters not hitting their marks. The compound was pramipexole. In less than seven days, improvement was seen. The jerky movements, trouble walking, and accompanying symptoms were almost completely gone after treatment.

The dopamine agonist was shown to nearly reverse all symptoms of the congenital dopamine transporter disease. Dopamine has proven once again how essential it is to the living system.

Reference:
Jennifer J. Rilstone, Reem A. Alkhater, Berge A. Minassian. Brain Dopamine–Serotonin Vesicular Transport Disease and Its Treatment. The New England Journal of Medicine, 2013.
http://dx.doi.org/10.1056/NEJMoa1207281