How Deep Brain Stimulation Affects Speech in Parkinsonís Disease
Emily Wang- firstname.lastname@example.org
1653 West Congress Parkway
Rush University Medical Center
Chicago, IL 60612
Popular version of paper 4aSC6
Presented Thursday morning, June
151st ASA Meeting, Providence, RI
The ability to speak has been believed to be unique to humans. However, for patients with Parkinsonís disease (PD), their ability to speak is affected by the disease, just like their ability to move their arms or to walk. This is because Parkinsonís disease causes motor impairment. It affects oneís motor functions due to the shortage of dopamine in the brain. The major symptoms such as resting tremor, rigidity, slow movement, and balance and coordination problems are treatable at early stages with medication such as Sinemet which provides the brain with dopamine. As the disease progresses, the symptoms may no longer controlled by medication and some patients start to experience drug-induced unwanted movements. The current treatment for advanced Parkinsonís disease is deep brain stimulation (DBS), a technique that involves placing a tiny electrode deep into the brain.
One of the stimulation targets is the subthalamic nucleus (STN). Many studies have shown that stimulation of STN bilaterally help PD patients with their limb movement such as walking and thus improve their quality of life. However, its effect on speech is unclear and some studies even reported that patients experienced speech problems after the surgical treatment.
From studying patients who had strokes or seizures, it is known that the damage to the left side brain usually causes more speech and language problems. This is because that 98% of the right handed people have their language center in their left hemisphere of the brain. Since the majority of PD patients have more severe symptoms on one side of the body, stimulating STN on one side of the brain provides a unique opportunity for studying the effects of left versus right STN DBS on speech.
We studied twenty right-handed PD patients who had STN DBS on one side of the brain only. Ten were operated on the right and ten on the left hemisphere. Both non-speech motor function and speech were evaluated three times: before surgery, and three-to-six months after surgery with stimulator turned off, and with stimulator turned on. All patients withdrew their PD medication for the testing. The stimulators were programmed as such that the examiners and patients did not know the stimulator condition during the two post-surgical testing. The patients were evaluated for their non-speech and speech functions.
The results showed that all 20 patients improved their non-speech motor functions with the use of stimulation regardless which side of the STN was stimulated. However, the improvement in speech function was not as impressive. The changes in speech function were also different between the two groups of patients depending on which side of the brain received the stimulation. For example, as a group, the patients who got right side brain stimulation showed improvement in their loudness and clarity of their speech; while the patients who had left side brain stimulation did not improve or even got worse. We also found that patients showed different level of deterioration in their speech function depending on the side of the brain the disease struck first even before the surgery took place.
The data suggest that careful documentation of baseline speech function is crucial for the interpretation of post-operative speech changes under different STN DBS conditions. Future studies should monitor both short-term and long-term effect of STN DBS on speech, and investigate how PD affects speech differently when the disease affects one side more than the other.
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