House of Mind

neurolove:

Another treatment for Parkinson’s: DBS

Deep brain stimulation (DBS) involves the implanting of electrodes in the brain that effectively “inactivate” a certain region.  It can be quite sophisticated, using multiple electrodes that can then have different patterns of stimulation.  There is a pacemaker that is implanted elsewhere in the body, usually where it can be removed to replace batteries and the like without too bad of side effects (so not in the brain tissue). 

In Parkinson’s, the electrodes are surgically implanted into the subthalamic nucleus (STN) or the internal segment of the globus pallidus (GPi).  For a refresher on the basal ganglia pathways, go here. STN excites GPi and GPi inhibits thalamus, both of which effectively decrease movements.  In Parkinson’s, patients are having trouble moving due to the decreased dopamine feeding into the basal ganglia loops.  Therefore, acting on STN or GPi and effectively inactivating those regions makes it so that movements will be easier.

It is also interesting to note that DBS can be used on other disorders, such as severe cases of obsessive-compulsive disorder (OCD) and Tourette’s Syndrome.  Tourette’s is characterised by motor and verbal tics that can be very intrusive, not what you usually see on TV (for instance, I know a patient whose uncontrollable tic is to poke their eye and they had blinded that eye with it).  DBS of the thalamus usually can be helpful for patients suffering from Tourette’s (I think you can figure out why it might be from what you know about the basal ganglia circuitry).

There are still more potential treatments for Parkinson’s that I will continue to discuss.

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neurolove:

Treatment for Parkinson’s : L-DOPA

The most obvious treatment for Parkinson’s would be to replace the dopamine in the brain that is being lost by dopaminergic neuron degeneration.  Dopamine itself, however, cannot pass the blood brain barrier to get into the brain.  L-DOPA, the precursor of dopamine (it is broken down to create dopamine), can pass the blood brain barrier however.  This means that we can administer L-DOPA, it will enter the brain, and then dopaminergic neurons with DOPA decarboxylase (the enzyme that breaks down L-DOPA) will convert L-DOPA into dopamine, giving the dopaminergic neurons that remain in the brain more dopamine to release and make up for the ones that have died.

This treatment works very well in the early stages of Parkinson’s.  Unfortunately, as time goes on, more and more L-DOPA is needed to help movement because more neurons are dying in the substantia nigra and there is a bit of tolerance to L-DOPA.  At the higher doses that are needed, there are much more dramatic side effects, including horrible hallucinations, twitches, obtrusive mood swings, etc.  Knowing what we know about the basal ganglia circuitry, we know that these are due to increased DA activating the direct pathway of the basal ganglia and increasing thoughts/emotions as well as movements.

Unfortunately, because of these side effects, L-DOPA is just a temporary treatment and cannot be used as long-term as needed for someone trying to live with Parkinson’s disease.  There are other possible treatments that I will discuss next.

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This post goes along nicely with the reblog about basal ganglia disorders. I think it’s important to say that L-DOPA isn’t just treatment, it’s an intermediary of an important catecholamine synthesis, as illustrated below…