Jerrold Vitek And Parkinson's Disease

Jerrold Vitek

Jerrold Vitek, MD, PhD was a 1984 graduate from the Medical School of University of Minnesota, which is where he obtained his Medial and Doctorate degree in Neurophysiology. Vitek completed his residency in Neurology in Maryland at the Johns Hopkins Hospital. In 1990, Vitek took a teaching position at The John Hopkins School of Medicine, which is a school known for their medical research and teaching. He only spent two years there, but spent his time examining motor systems in animals that modeled Parkinson’s and helped develop the Neurosurgery at the school. Then in 1990, Vitek started teaching at Emory University School of Medicine, located in Atlanta, Georgia, where he developed and directed the stereotactic neurosurgery

He is known for developing DBS improved treatment techniques for neurological diseases. It was during his time at Emory where he was underlying the benefits of DBS. It was not until Vitek worked as a physician at Cleveland Clinic where he started treating patient with DBS, developed new improvement for the application, and started DBS programming. This therapy treatment is for symptoms seen in Parkinson’s such as shaking, stiffness, and difficulty moving. Parkinson’s is a disease that affects the nervous system and movement. It is a neurodegenerative disease and is caused by certain nerve cells in the brain dying. These particular neurons produce the dopamine neurotransmitter and when they break down, dopamine levels decrease causing abnormal brain activity. “DBS Therapy uses a small, pacemaker-like device implanted under the skin in the chest (not in the brain). That device sends electronic signals through a very thin wire (called a lead) which is placed in the area of the brain that controls movement. These signals block some of the brain messages that cause the distracting and disabling motor symptoms associated with Parkinson's” (Health Central). DBS is typically used as a treatment when patients find that their medication is not as effective as it used to be, but not when it completely stops working. This procedure is also used to treat dystonia, a neurological

However, in 2008, Vitek did a study on DBS and whether the mechanisms are an excitation or inhibition. In the beginning, it was believed that DBS suppresses neuronal activity by depressing output from the stimulated sites in the brain, the sub thalamic nucleus (STN) and globus pallidus (GPi). During micro dialysis of the GPi, researchers found increased levels of glutamate during STN stimulation, which is an excitatory neurotransmitter. There was as study done on monkeys that showed an increased-mean discharge of neurons in the GPi during DBS stimulation in the STN, which improved the motor signs that are seen in Parkinson’s. “This hypothesis would suggest that, although high-frequency stimulation may inhibit neurons, the output from that structure may still be increased as the result of axon activation. As a result, if one stimulates and records in the same structure, you may find inhibition of neuronal activity, although output from the stimulated structure may actually be increased” (Mechanisms of deep brain stimulation: Excitation or inhibition). In other words, an improvement in bradykinesia, abnormal slow movement, and rigidity in Parkinson’s correspond with increased mean discharge rates of neurons in GPi (neurons were firing at faster